Anorexia nervosa

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Anorexia nervosa
Other namesAnorexia
Gull - Anorexia Miss A.jpg
"Miss A—" depicted in 1866 and in 1870 after treatment. Her condition was one of the earliest case studies of anorexia, published in medical research papers of William Gull.
Specialty Psychiatry, clinical psychology
Symptoms Fear of gaining weight, strong desire to be thin, food restrictions, [1] body image disturbance
Complications Osteoporosis, infertility, heart damage, suicide, [1] whole-body swelling (edema), heart failure and/or lung failure, gastrointestinal problems, extensive muscle weakness, delirium, death [2]
Usual onsetAdolescence to early adulthood [1]
CausesUnknown [3]
Risk factors Family history, high-level athletics, bullying, social media, modelling, substance use disorder, being a dancer or gymnast [3] [4] [5]
Differential diagnosis Body dysmorphic disorder, bulimia nervosa, hyperthyroidism, inflammatory bowel disease, dysphagia, cancer [6] [7]
Treatment Cognitive behavioral therapy, hospitalisation to restore weight [1] [8]
Prognosis 5% risk of death over 10 years [4] [9]
Frequency2.9 million (2015) [10]
Deaths600 (2015) [11]

Anorexia nervosa (AN), often referred to simply as anorexia, [12] is an eating disorder characterized by food restriction, body image disturbance, fear of gaining weight, and an overpowering desire to be thin. [1]

Contents

Individuals with anorexia nervosa have a fear of being overweight or being seen as such, despite the fact that they are typically underweight. [1] [3] The DSM-5 describes this perceptual symptom as "disturbance in the way in which one's body weight or shape is experienced". [8] In research and clinical settings, this symptom is called "body image disturbance". [13] Individuals with anorexia nervosa also often deny that they have a problem with low weight. [4] They may weigh themselves frequently, eat small amounts, and only eat certain foods. [1] Some exercise excessively, force themselves to vomit (in the "anorexia purging" subtype), or use laxatives to lose weight and control body shapes, and/or binge eat. [1] Medical complications may include osteoporosis, infertility, and heart damage, [1] along with the cessation of menstrual periods. [4] In extreme cases, patients with anorexia nervosa who continually refuse significant dietary intake and weight restoration interventions, and are declared to lack capacity to make decisions by a psychiatrist, may be fed by force under restraint via nasogastric tube [14] after asking their parents or proxies [15] to make the decision for them. [16]

Anorexia often develops during adolescence or young adulthood, [1] typically following a major life-change or stress-inducing event. [4] The causes of anorexia are varied and may differ from individual to individual. [3] There is emerging evidence that there is a genetic component, with identical twins more often affected than fraternal twins. [3] Cultural factors also appear to play a role, with societies that value thinness having higher rates of the disease. [4] Anorexia also commonly occurs in athletes who play sports where a low bodyweight is thought to be advantageous for aesthetics or performance, such as dance, gymnastics, running, and figure skating. [4] [5] [17]

Treatment of anorexia involves restoring the patient back to a healthy weight, treating their underlying psychological problems, and addressing underlying maladaptive behaviors. [1] While medications do not help with weight gain, they may be used to help with associated anxiety or depression. [1] Different therapy methods may be useful, such as cognitive behavioral therapy or an approach where parents assume responsibility for feeding their child, known as Maudsley family therapy. [1] [18] Sometimes people require admission to a hospital to restore weight. [8] Evidence for benefit from nasogastric tube feeding is unclear. [19] Such an intervention may be highly distressing for both anorexia patients and healthcare staff when administered against the patient's will under restraint. [14] Some people with anorexia will have a single episode and recover while others may have recurring episodes over years. [8] Many complications, both physical and psychological, improve or resolve with nutritional rehabilitation and adequate weight gain. [8]

It is estimated to occur in 0.3% to 4.3% of women and 0.2% to 1% of men in Western countries at some point in their life. [20] About 0.4% of young women are affected in a given year and it is estimated to occur ten times more commonly among women than men. [4] [20] It is unclear whether the increased incidence of anorexia observed in the 20th and 21st centuries is due to an actual increase in its frequency or simply due to improved diagnostic capabilities. [3] In 2013, it directly resulted in about 600 deaths globally, up from 400 deaths in 1990. [21] Eating disorders also increase a person's risk of death from a wide range of other causes, including suicide. [1] [20] About 5% of people with anorexia die from complications over a ten-year period. [4] [9]

Signs and symptoms

The back of a person with anorexia Louis Bataille, 'Deux cas d'anorexie hysterique' Wellcome L0020548 (backcropped).jpg
The back of a person with anorexia

Anorexia nervosa is an eating disorder characterized by attempts to lose weight by way of starvation. A person with anorexia nervosa may exhibit a number of signs and symptoms, the type and severity of which may vary and be present but not readily apparent. [22] Though anorexia is typically recognized by the physical manifestations of the illness, it is a mental disorder that can be present at any weight.

Anorexia nervosa, and the associated malnutrition that results from self-imposed starvation, can cause complications in every major organ system in the body. [23] Hypokalemia, a drop in the level of potassium in the blood, is a sign of anorexia nervosa. [24] [25] A significant drop in potassium can cause abnormal heart rhythms, constipation, fatigue, muscle damage, and paralysis. [26]

Signs and symptoms may be classified in various categories including: physical, cognitive, affective, behavioral and perceptual:

Physical symptoms

Cognitive symptoms

Affective symptoms

Behavioral symptoms

Perceptual symptoms

Interoception

Interoception involves the conscious and unconscious sense of the internal state of the body, and it has an important role in homeostasis and regulation of emotions. [41] Aside from noticeable physiological dysfunction, interoceptive deficits also prompt individuals with anorexia to concentrate on distorted perceptions of multiple elements of their body image. [42] This exists in both people with anorexia and in healthy individuals due to impairment in interoceptive sensitivity and interoceptive awareness. [42]

Aside from weight gain and outer appearance, people with anorexia also report abnormal bodily functions such as indistinct feelings of fullness. [43] This provides an example of miscommunication between internal signals of the body and the brain. Due to impaired interoceptive sensitivity, powerful cues of fullness may be detected prematurely in highly sensitive individuals, which can result in decreased calorie consumption and generate anxiety surrounding food intake in anorexia patients. [44] People with anorexia also report difficulty identifying and describing their emotional feelings and the inability to distinguish emotions from bodily sensations in general, called alexithymia. [43]

Interoceptive awareness and emotion are deeply intertwined, and could mutually impact each other in abnormalities. [44] Anorexia patients also exhibit emotional regulation difficulties that ignite emotionally-cued eating behaviors, such as restricting food or excessive exercising. [44] Impaired interoceptive sensitivity and interoceptive awareness can lead anorexia patients to adapt distorted interpretations of weight gain that are cued by physical sensations related to digestion (e.g., fullness). [44] Combined, these interoceptive and emotional elements could together trigger maladaptive and negatively reinforced behavioral responses that assist in the maintenance of anorexia. [44] In addition to metacognition, people with anorexia also have difficulty with social cognition including interpreting others' emotions, and demonstrating empathy. [45] Abnormal interoceptive awareness and interoceptive sensitivity shown through all of these examples have been observed so frequently in anorexia that they have become key characteristics of the illness. [43]

Comorbidity

Other psychological issues may factor into anorexia nervosa. Some pre-existing disorders can increase a person's likelihood to develop an eating disorder. Additionally, Anorexia Nervosa can contribute to the development of certain conditions. [46] The presence of psychiatric comorbidity has been shown to affect the severity and type of anorexia nervosa symptoms in both adolescents and adults. [47]

Obsessive-compulsive disorder (OCD) and obsessive-compulsive personality disorder (OCPD) are highly comorbid with AN. [48] [49] OCD is linked with more severe symptomatology and worse prognosis. [50] The causality between personality disorders and eating disorders has yet to be fully established. [51] Other comorbid conditions include depression, [52] alcoholism, [53] borderline and other personality disorders, [54] [55] anxiety disorders, [56] attention deficit hyperactivity disorder, [57] and body dysmorphic disorder (BDD). [58] Depression and anxiety are the most common comorbidities, [59] and depression is associated with a worse outcome. [59] Autism spectrum disorders occur more commonly among people with eating disorders than in the general population. [60] Zucker et al. (2007) proposed that conditions on the autism spectrum make up the cognitive endophenotype underlying anorexia nervosa and appealed for increased interdisciplinary collaboration. [61]

Causes

Dysregulation of the serotonin pathways has been implicated in the cause and mechanism of anorexia. Dopamine and serotonin pathways.png
Dysregulation of the serotonin pathways has been implicated in the cause and mechanism of anorexia.

There is evidence for biological, psychological, developmental, and sociocultural risk factors, but the exact cause of eating disorders is unknown. [62]

Genetic

Genetic correlations of anorexia with psychiatric and metabolic traits Association of Anorexia nervosa with psychiatric and metabolic traits.jpg
Genetic correlations of anorexia with psychiatric and metabolic traits

Anorexia nervosa is highly heritable. [62] Twin studies have shown a heritability rate of 28–58%. [63] First-degree relatives of those with anorexia have roughly 12 times the risk of developing anorexia. [64] Association studies have been performed, studying 128 different polymorphisms related to 43 genes including genes involved in regulation of eating behavior, motivation and reward mechanics, personality traits and emotion. Consistent associations have been identified for polymorphisms associated with agouti-related peptide, brain derived neurotrophic factor, catechol-o-methyl transferase, SK3 and opioid receptor delta-1. [65] Epigenetic modifications, such as DNA methylation, may contribute to the development or maintenance of anorexia nervosa, though clinical research in this area is in its infancy. [66] [67]

A 2019 study found a genetic relationship with mental disorders, such as schizophrenia, obsessive–compulsive disorder, anxiety disorder and depression; and metabolic functioning with a negative correlation with fat mass, type 2 diabetes and leptin. [68]

Environmental

Obstetric complications: prenatal and perinatal complications may factor into the development of anorexia nervosa, such as preterm birth, [69] maternal anemia, diabetes mellitus, preeclampsia, placental infarction, and neonatal heart abnormalities. [70] Neonatal complications may also have an influence on harm avoidance, one of the personality traits associated with the development of AN. [71]

Neuroendocrine dysregulation: altered signaling of peptides that facilitate communication between the gut, brain and adipose tissue, such as ghrelin, leptin, neuropeptide Y and orexin, may contribute to the pathogenesis of anorexia nervosa by disrupting regulation of hunger and satiety. [72] [73]

Gastrointestinal diseases: people with gastrointestinal disorders may be more at risk of developing disorders of eating practices than the general population, principally restrictive eating disturbances. [74] An association of anorexia nervosa with celiac disease has been found. [75] The role that gastrointestinal symptoms play in the development of eating disorders seems rather complex. Some authors report that unresolved symptoms prior to gastrointestinal disease diagnosis may create a food aversion in these persons, causing alterations to their eating patterns. [76] Other authors report that greater symptoms throughout their diagnosis led to greater risk. [77] It has been documented that some people with celiac disease, irritable bowel syndrome or inflammatory bowel disease who are not conscious about the importance of strictly following their diet, choose to consume their trigger foods to promote weight loss. [78] On the other hand, individuals with good dietary management may develop anxiety, food aversion and eating disorders because of concerns around cross contamination of their foods. [79] [74] Some authors suggest that medical professionals should evaluate the presence of an unrecognized celiac disease in all people with eating disorder, especially if they present any gastrointestinal symptom (such as decreased appetite, abdominal pain, bloating, distension, vomiting, diarrhea or constipation), weight loss, or growth failure; and also routinely ask celiac patients about weight or body shape concerns, dieting or vomiting for weight control, to evaluate the possible presence of eating disorders, [75] especially in women. [80]

Anorexia nervosa is more likely to occur in a person's pubertal years. Some explanatory hypotheses for the rising prevalence of eating disorders in adolescence are "increase of adipose tissue in girls, hormonal changes of puberty, societal expectations of increased independence and autonomy that are particularly difficult for anorexic adolescents to meet; [and] increased influence of the peer group and its values." [81]

Anorexia as adaptation

Studies have hypothesized that disordered eating patterns may be epiphenomena of starvation. The results of the Minnesota Starvation Experiment, for example, showed that normal controls will exhibit many of the same behavioral patterns associated with AN when subjected to starvation. Similarly, scientific experiments conducted using mice have suggested that other mammals exhibit these same behaviors, especially compulsive movement, when caloric restriction is induced, [82] likely mediated by various changes in the neuroendocrine system. [83] [84] [85] This has given further rise to the hypothesis that anorexia nervosa and other restrictive eating disorders may be an evolutionarily advantageous adaptive response to a perceived famine in the environment. [86] [87]

Psychological

Early theories of the cause of anorexia linked it to childhood sexual abuse or dysfunctional families; [88] [89] evidence is conflicting, and well-designed research is needed. [62] The fear of food is known as sitiophobia [90] or cibophobia, [91] and is part of the differential diagnosis. [92] [93] Other psychological causes of anorexia include low self-esteem, feeling like there is lack of control, depression, anxiety, and loneliness. [94] People with anorexia are, in general, highly perfectionistic [95] and most have obsessive compulsive personality traits [96] which may facilitate sticking to a restricted diet. [97] It has been suggested that patients with anorexia are rigid in their thought patterns, and place a high level of importance upon being thin. [98] [99]

Although the prevalence rates vary greatly, between 37% and 100%, [100] there appears to be a link between traumatic events and eating disorder diagnosis. [101] Approximately 72% of individuals with anorexia report experiencing a traumatic event prior to the onset of eating disorder symptoms, with binge-purge subtype reporting the highest rates. [100] [101] There are many traumatic events that have been identified as possible risk factors for the development of anorexia, the first of which was childhood sexual abuse. [102] However, other traumatic events, such as physical and emotional abuse have also been found to be risk factors. Interpersonal, as opposed to non-interpersonal trauma, has been seen as the most common type of traumatic event, [100] which can encompass sexual, physical, and emotional abuse. [102] Individuals who experience repeated trauma, like those who experience trauma perpetrated by a caregiver or loved one, have increased symptom severity of anorexia and a greater prevalence of comorbid psychiatric diagnoses. [102]

In individuals with anorexia, the prevalence rates for those who also qualify for a PTSD diagnosis ranges from 4% to 52% in non-clinical samples to 10% to 47% in clinical samples. [100] [ non-primary source needed ] [101] [ non-primary source needed ] A complicated symptom profile develops when trauma and anorexia meld; the bodily experience of the individual is changed and intrusive thoughts and sensations may be experienced. [102] Traumatic events can lead to intrusive and obsessive thoughts, and the symptom of anorexia that has been most closely linked to a PTSD diagnosis is increased obsessive thoughts pertaining to food. [102] Similarly, impulsivity is linked to the purge and binge-purge subtypes of anorexia, trauma, and PTSD. [101] Emotional trauma (e.g., invalidation, chaotic family environment in childhood) may lead to difficulty with emotions, particularly the identification of and how physical sensations contribute to the emotional response. [102]

When trauma is perpetrated on an individual, it can lead to feelings of not being safe within their own body. [102] Both physical and sexual abuse can lead to an individual seeing their body as belonging to an "other" and not to the "self". [102] Individuals who feel as though they have no control over their bodies due to trauma may use food as a means of control because the choice to eat is an unmatched expression of control. [102] By exerting control over food, individuals can choose when to eat and how much to eat. Individuals, particularly children experiencing abuse, may feel a loss of control over their life, circumstances, and their own bodies. Particularly sexual abuse, but also physical abuse, can make individuals feel that the body is not a safe place and an object over which another has control. Starvation, in the case of anorexia, may also lead to reduction in the body as a sexual object, making starvation a solution. Restriction may also be a means by which the pain an individual is experiencing can be communicated. [102]

Sociological

Anorexia nervosa has been increasingly diagnosed since 1950; [103] the increase has been linked to vulnerability and internalization of body ideals. [81] People in professions where there is a particular social pressure to be thin (such as models and dancers) were more likely to develop anorexia, [104] and those with anorexia have much higher contact with cultural sources that promote weight loss. [105] This trend can also be observed for people who partake in certain sports, such as jockeys and wrestlers. [106] There is a higher incidence and prevalence of anorexia nervosa in sports with an emphasis on aesthetics, where low body fat is advantageous, and sports in which one has to make weight for competition. [107] Family group dynamics can play a role in the perpetuation of anorexia including negative expressed emotion in overprotective families where blame is frequently experienced among its members. [108] [109] [110] In the face of constant pressure to be thin, often perpetuated by teasing and bullying, feelings of low self-esteem and self-worth can arise, including the perception that one is not "deserving" of food. [94]

Media effects

Persistent exposure to media that present thin ideal may constitute a risk factor for body dissatisfaction and anorexia nervosa. Cultures that equate thinness with beauty often have higher rates of anorexia nervosa. [111] The cultural ideal for body shape for men versus women continues to favor slender women and athletic, V-shaped muscular men. Media sources such as magazines, television shows, and social media can contribute to body dissatisfaction and disordered eating across the globe, by emphasizing Western ideals of slimness. [112] A 2002 review found that, of the magazines most popular among people aged 18 to 24 years, those read by men, unlike those read by women, were more likely to feature ads and articles on shape than on diet. [113] Body dissatisfaction and internalization of body ideals are risk factors for anorexia nervosa that threaten the health of both male and female populations. [114]

Another online aspect contributing to higher rates of eating disorders such as anorexia nervosa are websites and communities on social media that stress the importance of attainment of body ideals extol. These communities promote anorexia nervosa through the use of religious metaphors, lifestyle descriptions, "thinspiration" or "fitspiration" (inspirational photo galleries and quotes that aim to serve as motivators for attainment of body ideals). [115] [116] Pro-anorexia websites reinforce internalization of body ideals and the importance of their attainment. [116]

Cultural

Cultural attitudes towards body image, beauty, and health also significantly impact the incidence of anorexia nervosa. There is a stark contrast between Western societies that idolize slimness and certain Eastern traditions that worship gods depicted with larger bodies, [117] and these varying cultural norms have varying influences on eating behaviors, self-perception, and anorexia in their respective cultures. For example, despite the fact that "fat phobia", or a fear of fat, is a key diagnostic criteria of anorexia by the DSM-5, anorexic patients in Asia rarely display this trait, as deep-rooted cultural values in Asian cultures praise larger bodies. [118] Fat phobia appears to be intricately linked to Western culture, encompassing how various cultural perceptions impact anorexia in various ways. It calls on the need for greater, diverse cultural consideration when looking at the diagnosis and experience of anorexia. For instance, in a cross-sectional study done on British South Asian adolescent English adolescent anorexia patients, it was found that both patients' symptom profiles differed. South Asians were less likely to exhibit fat-phobia as a symptom versus their English counterparts, instead exhibiting loss of appetite. However, both kinds of patients had distorted body images, implying the possibility of disordered eating and highlighting the need for cultural sensitivity when diagnosing anorexia. [119]

Notably, although these cultural distinctions persist, modernization and globalization slowly homogenize these attitudes. [117] Anorexia is increasingly tied to the pressures of a global culture that celebrates Western ideals of thinness. The spread of Western media, fashion, and lifestyle ideals across the globe has begun to shift perceptions and standards of beauty in diverse cultures, contributing to a rise in the incidence of anorexia in places they were once rare in. [120] Anorexia, once primarily associated with Western culture, seems more than ever to be linked to the cultures of modernity and globalization.

Mechanisms

Evidence from physiological, pharmacological and neuroimaging studies suggest serotonin (also called 5-HT) may play a role in anorexia. While acutely ill, metabolic changes may produce a number of biological findings in people with anorexia that are not necessarily causative of the anorexic behavior. For example, abnormal hormonal responses to challenges with serotonergic agents have been observed during acute illness, but not recovery. Nevertheless, increased cerebrospinal fluid concentrations of 5-hydroxyindoleacetic acid (a metabolite of serotonin), and changes in anorectic behavior in response to acute tryptophan depletion (tryptophan is a metabolic precursor to serotonin) support a role in anorexia. The activity of the 5-HT2A receptors has been reported to be lower in patients with anorexia in a number of cortical regions, evidenced by lower binding potential of this receptor as measured by PET or SPECT, independent of the state of illness. While these findings may be confounded by comorbid psychiatric disorders, taken as a whole they indicate serotonin in anorexia. [121] [122] These alterations in serotonin have been linked to traits characteristic of anorexia such as obsessiveness, anxiety, and appetite dysregulation. [85]

Neuroimaging studies investigating the functional connectivity between brain regions have observed a number of alterations in networks related to cognitive control, introspection, and sensory function. Alterations in networks related to the dorsal anterior cingulate cortex may be related to excessive cognitive control of eating related behaviors. Similarly, altered somatosensory integration and introspection may relate to abnormal body image. [123] A review of functional neuroimaging studies reported reduced activations in "bottom up" limbic region and increased activations in "top down" cortical regions which may play a role in restrictive eating. [124]

Compared to controls, people who have recovered from anorexia show reduced activation in the reward system in response to food, and reduced correlation between self reported liking of a sugary drink and activity in the striatum and anterior cingulate cortex. Increased binding potential of 11C radiolabelled raclopride in the striatum, interpreted as reflecting decreased endogenous dopamine due to competitive displacement, has also been observed. [125]

Structural neuroimaging studies have found global reductions in both gray matter and white matter, as well as increased cerebrospinal fluid volumes. Regional decreases in the left hypothalamus, left inferior parietal lobe, right lentiform nucleus and right caudate have also been reported [126] in acutely ill patients. However, these alterations seem to be associated with acute malnutrition and largely reversible with weight restoration, at least in nonchronic cases in younger people. [127] In contrast, some studies have reported increased orbitofrontal cortex volume in currently ill and in recovered patients, although findings are inconsistent. Reduced white matter integrity in the fornix has also been reported. [128]

Diagnosis

A diagnostic assessment includes the person's current circumstances, biographical history, current symptoms, and family history. The assessment also includes a mental state examination, which is an assessment of the person's current mood and thought content, focusing on views on weight and patterns of eating.

DSM-5

Anorexia nervosa is classified under the Feeding and Eating Disorders in the latest revision of the Diagnostic and Statistical Manual of Mental Disorders (DSM 5). There is no specific BMI cut-off that defines low weight required for the diagnosis of anorexia nervosa. [129] [4]

The diagnostic criteria for anorexia nervosa (all of which needing to be met for diagnosis) are: [8] [130]

Relative to the previous version of the DSM (DSM-IV-TR), the 2013 revision (DSM5) reflects changes in the criteria for anorexia nervosa. Most notably, the amenorrhea (absent period) criterion was removed. [8] [131] Amenorrhea was removed for several reasons: it does not apply to males, it is not applicable for females before or after the age of menstruation or taking birth control pills, and some women who meet the other criteria for AN still report some menstrual activity. [8]

Subtypes

There are two subtypes of AN: [23] [132]

  • Binge-eating/purging type: patients with anorexia could show binge eating and purging behavior. [132] It is different from bulimia nervosa in terms of the individual's weight. An individual with binge-eating/purging type anorexia is usually significantly underweight. People with bulimia nervosa on the other hand can sometimes be normal-weight or overweight. [33]
  • Restricting type: the individual uses restricting food intake, fasting, diet pills, or exercise as a means for losing weight; [23] they may exercise excessively to keep off weight or prevent weight gain, and some individuals eat only enough to stay alive. [23] [33] In the restrictive type, there are no recurrent episodes of binge-eating or purging present. [129]

Levels of severity

Body mass index (BMI) is used by the DSM-5 as an indicator of the level of severity of anorexia nervosa. The DSM-5 states these as follows: [133]

  • Mild: BMI of greater than 17
  • Moderate: BMI of 16–16.99
  • Severe: BMI of 15–15.99
  • Extreme: BMI of less than 15

Investigations

Medical tests to check for signs of physical deterioration in anorexia nervosa may be performed by a general physician or psychiatrist, including:

Differential diagnoses

A variety of medical and psychological conditions have been misdiagnosed as anorexia nervosa; in some cases the correct diagnosis was not made for more than ten years.

The distinction between binge purging anorexia, bulimia nervosa and Other Specified Feeding or Eating Disorders (OSFED) is often difficult for non-specialist clinicians. A main factor differentiating binge-purge anorexia from bulimia is the gap in physical weight. Patients with bulimia nervosa are ordinarily at a healthy weight, or slightly overweight. Patients with binge-purge anorexia are commonly underweight. [148] Moreover, patients with the binge-purging subtype may be significantly underweight and typically do not binge-eat large amounts of food. [148] In contrast, those with bulimia nervosa tend to binge large amounts of food. [148] It is not unusual for patients with an eating disorder to "move through" various diagnoses as their behavior and beliefs change over time. [61]

Gender difference

While anorexia nervosa is commonly associated with women, it can also affect men. However, the diagnosis and awareness of eating disorders and associated health risks in men are frequently underrepresented. A survey conducted among a randomly selected sample of individuals aged 18–35 reveals that females are more inclined to report behaviors such as fasting, body checking, and body avoidance, whereas males are more prone to report overeating. [149] 0.3% of men may experience anorexia nervosa in their life time. [150]

Treatment

Treatment for people with anorexia nervosa should be individualized and tailored to each person's medical, psychological, and nutritional circumstances. Treating this condition with an interdisciplinary team is suggested so that the different health care professional specialties can help addresses the different challenges that can be associated with recovery. [151] Treatment for anorexia typically involves a combination of medical, psychological interventions such as therapy, and nutritional interventions (diet) interventions. Hospitalization may also be needed in some cases, [152] and the person requires a comprehensive medical assessment to help direct the treatment options. There is no conclusive evidence that any particular treatment approach for anorexia nervosa works better than others. [12] [153] In some clinical settings a specific body image intervention is performed to reduce body dissatisfaction and body image disturbance. Although restoring the person's weight is the primary task at hand, optimal treatment also includes and monitors behavioral change in the individual as well. [19]

In general, treatment for anorexia nervosa aims to address three main areas: [154]

Psychological support

Psychological support, often in the form of cognitive-behavioral therapy (CBT), family-bases treatment, or psychotherapy aims to change distorted thoughts and behaviors around food, body image, and self-worth, with family-based therapy also being a key approach for younger patients.

Family-based therapy

Family-based treatment (FBT) may be more successful than individual therapy for adolescents with AN. [9] [155] Various forms of family-based treatment have been proven to work in the treatment of adolescent AN including conjoint family therapy (CFT), in which the parents and child are seen together by the same therapist, and separated family therapy (SFT) in which the parents and child attend therapy separately with different therapists. [9] Proponents of family therapy for adolescents with AN assert that it is important to include parents in the adolescent's treatment. [9] The evidence supporting family based therapy for adults is weak and despite the evidence that it is effective and the primary choice for treatment in adolescents, there is no evidence it is helpful for adults. [12] [156] [157] A four- to five-year follow up study of the Maudsley family therapy, an evidence-based manualized model, showed full recovery at rates up to 90%. [158] The Maudsley model of family therapy is problem focused, and the treatment targets re-establishing regular eating, weight restoration, and the reduction of illness behaviors like purging. [159] The Maudsley model is split into three phases, with phase one focusing on the parents implementing weight restoration in the child; phase two transitioning control over food back to the individual at an age-appropriate level; and phase three focusing on other issues related to typical adolescent development (e.g., social and other psychological developments), and helps parents learn how to interact with their child. [159] Although this model is recommended by the National Institute of Mental Health (NIMH), [160] critics claim that it has the potential to create power struggles in an intimate relationship and may disrupt equal partnerships. [158]

Cognitive behavioral therapy

Cognitive behavioral therapy (CBT) is useful in adolescents and adults with anorexia nervosa. [161] One of the most known psychotherapy in the field is CBT-E, an enhanced cognitive-behavior therapy specifically focus to eating disorder psychopathology. Acceptance and commitment therapy is a third-wave cognitive-behavioral therapy which has shown promise in the treatment of AN. [162] Cognitive remediation therapy (CRT) is also used in treating anorexia nervosa. [163] Schema-Focused Therapy (a form of CBT) was developed by Dr. Jeffrey Young and is effective in helping patients identify origins and triggers for disordered eating. [164]

Psychotherapy

Psychotherapy for individuals with AN is challenging as they may value being thin and may seek to maintain control and resist change. [165] Initially, developing a desire to change is fundamental. [166] There is no strong evidence to suggest one type of psychotherapy over another for treating anorexia nervosa in adults or adolescents. [151]

Diet

Diet is the most essential factor to work on in people with anorexia nervosa, and must be tailored to each person's needs. Food variety is important when establishing meal plans as well as foods that are higher in energy density, especially in carbohydrates and dietary fat, which are easier for the undernourished body to break down. [167] Evidence of a role for zinc supplementation during refeeding is unclear. [19]

Historically, practitioners have slowly increased calories at a measured pace from a starting point of around 1,200 kcal/day. [38] [168] However, as understanding of the process of weight restoration has improved, an approach that favors a higher starting point and a more rapid rate of increase has become increasingly common. In either approach, the end goal is typically in the range of 3,000 to 3,500 kcal/day. [168] People who experience hypermetabolism in response to refeeding have higher caloric intake needs. [169]

Extreme hunger

People who have undergone significant caloric deficits often report experiencing hyperphagia, or extreme hunger. With adequate refeeding and the full restoration of both fat mass and fat-free mass, hunger eventually becomes normalized. However, the restoration of fat-free mass typically takes longer than that of body fat, leading to "fat overshoot" or "overshoot weight," wherein the patient's body fat levels are greater than pre-starvation levels. [170] The timeline of the complete normalization of hunger varies considerably from individual to individual, from a few months to multiple years. [171]

Refeeding syndrome

Treatment professionals tend to be conservative with refeeding in anorexic patients due to the risk of refeeding syndrome (RFS), which occurs when a malnourished person is refed too quickly for their body to be able to adapt. Two of the most common indicators that RFS is occurring are low phosophate levels and low potassium levels. [172] RFS is most likely to happen in severely or extremely underweight anorexics, as well as when medical comorbidities, such as infection or cardiac failure, are present. In these circumstances, it is recommended to start refeeding more slowly but to build up rapidly as long as RFS does not occur. Recommendations on energy requirements in the most medically compromised patients vary, from 5–10 kcal/kg/day to 1900 kcal/day. [173] [174] This risk-averse approach can lead to underfeeding, which results in poorer outcomes for short- and long-term recovery. [168]

Medication

Pharmaceuticals have limited benefit for anorexia itself. [175] [129] There is a lack of good information from which to make recommendations concerning the effectiveness of antidepressants in treating anorexia. [176] Administration of olanzapine has been shown to result in a modest but statistically significant increase in body weight of anorexia nervosa patients. [177]

Admission to hospital

Patients with AN may be deemed to have a lack of insight regarding the necessity of treatment, and thus may be involuntarily treated without their consent. [152] :1038 AN has a high mortality and patients admitted in a severely ill state to medical units are at particularly high risk. [178] Diagnosis can be challenging, risk assessment may not be performed accurately, consent and the need for compulsion may not be assessed appropriately, refeeding syndrome may be missed or poorly treated and the behavioural and family problems in AN may be missed or poorly managed. [179] Guidelines published by the Royal College of Psychiatrists recommend that medical and psychiatric experts work together in managing severely ill people with AN. [180]

Experience of treatment

Patients involved in treatment sometimes felt that treatment focused on biological aspects of body weight and eating behaviour change rather than their perceptions or emotional state. [181] :8 Patients felt that a therapists trust in them shown by being treated as a complete person with their own capacities was significant. [181] :9 Some patients defined recovery from AN in terms of reclaiming a lost identity. [181] :10 Additionally, access to timely treatment can be hindered by systemic challenges within the medical system. Some individuals have reported experiencing delays in treatment, particularly when transitioning from adolescence to adulthood. [182] It has been noted that once patients reach the age of 17, they may encounter obstacles in receiving continued care, with treatment resuming only after they turn 18. This delay can exacerbate the severity of the disorder.

Healthcare workers involved in the treatment of anorexia reported frustration and anger to setbacks in treatment and noncompliance and were afraid of patients dying. Some healthcare workers felt that they did not understand the treatment and that medical doctors were making decisions. [183] :11 They may feel powerless to improve a patient's situation and deskilled as a result. [183] :12 Healthcare workers involved in monitoring patients consumption of food felt watched themselves. [183] :12 Healthcare workers often feel a degree of moral dissonance of not being in control of outcomes which they may protect against by focusing on individual tasks, avoiding identifying with patients (for example by making their eating behavior very different and not sharing personal information with patients), and blaming patients for their distress. [183] :13,14 Healthcare workers would inflexibly follow process to avoid responsibility. [183] :13 Healthcare workers attempted to reach balance by gradually giving patients back control avoiding feeling sole responsibility for outcomes, being mindful of their emotional state, and trying to view eating disorders as external from patients. [183] :13

Prognosis

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AN has the highest mortality rate of any psychological disorder. [9] The mortality rate is 11 to 12 times greater than in the general population, and the suicide risk is 56 times higher. [24] Half of women with AN achieve a full recovery, while an additional 20–30% may partially recover. [9] [24] Not all people with anorexia recover completely: about 20% develop anorexia nervosa as a chronic disorder. [153] If anorexia nervosa is not treated, serious complications such as heart conditions [22] and kidney failure can arise and eventually lead to death. [184] The average number of years from onset to remission of AN is seven for women and three for men. After ten to fifteen years, 70% of people no longer meet the diagnostic criteria, but many still continue to have eating-related problems. [185]

Alexithymia (inability to identify and describe one's own emotions) influences treatment outcome. [175] Recovery is also viewed on a spectrum rather than black and white. According to the Morgan-Russell criteria, individuals can have a good, intermediate, or poor outcome. Even when a person is classified as having a "good" outcome, weight only has to be within 15% of average, and normal menstruation must be present in females. The good outcome also excludes psychological health. Recovery for people with anorexia nervosa is undeniably positive, but recovery does not mean a return to normal. [186]

Complications

Anorexia nervosa can have serious implications if its duration and severity are significant and if onset occurs before the completion of growth, pubertal maturation, or the attainment of peak bone mass. [187] [ medical citation needed ] Complications specific to adolescents and children with anorexia nervosa can include the following: Growth retardation may occur, as height gain may slow and can stop completely with severe weight loss or chronic malnutrition. In such cases, provided that growth potential is preserved, height increase can resume and reach full potential after normal intake is resumed. [188] Height potential is normally preserved if the duration and severity of illness are not significant or if the illness is accompanied by delayed bone age (especially prior to a bone age of approximately 15 years), as hypogonadism may partially counteract the effects of undernutrition on height by allowing for a longer duration of growth compared to controls.[ medical citation needed ] Appropriate early treatment can preserve height potential, and may even help to increase it in some post-anorexic subjects, due to factors such as long-term reduced estrogen-producing adipose tissue levels compared to premorbid levels.[ medical citation needed ] In some cases, especially where onset is before puberty, complications such as stunted growth and pubertal delay are usually reversible. [189]

Anorexia nervosa causes alterations in the female reproductive system; significant weight loss, as well as psychological stress and intense exercise, typically results in a cessation of menstruation in women who are past puberty. In patients with anorexia nervosa, there is a reduction of the secretion of gonadotropin releasing hormone in the central nervous system which prevents ovulation. [190] Anorexia nervosa can also result in pubertal delay or arrest. Both height gain and pubertal development are dependent on the release of growth hormone and gonadotropins (LH and FSH) from the pituitary gland. Suppression of gonadotropins in people with anorexia nervosa has been documented. [191] Typically, growth hormone (GH) levels are high, but levels of IGF-1, the downstream hormone that should be released in response to GH are low; this indicates a state of "resistance" to GH due to chronic starvation. [192] IGF-1 is necessary for bone formation, and decreased levels in anorexia nervosa contribute to a loss of bone density and potentially contribute to osteopenia or osteoporosis. [192] Anorexia nervosa can also result in reduction of peak bone mass. Buildup of bone is greatest during adolescence, and if onset of anorexia nervosa occurs during this time and stalls puberty, low bone mass may be permanent. [193]

Hepatic steatosis, or fatty infiltration of the liver, can also occur, and is an indicator of malnutrition in children. [194] Neurological disorders that may occur as complications include seizures and tremors. Wernicke encephalopathy, which results from vitamin B1 deficiency, has been reported in patients who are extremely malnourished; symptoms include confusion, problems with the muscles responsible for eye movements and abnormalities in walking gait.

The most common gastrointestinal complications of anorexia nervosa are delayed stomach emptying and constipation, but also include elevated liver function tests, diarrhea, acute pancreatitis, heartburn, difficulty swallowing, and, rarely, superior mesenteric artery syndrome. [195] Delayed stomach emptying, or gastroparesis, often develops following food restriction and weight loss; the most common symptom is bloating with gas and abdominal distension, and often occurs after eating. Other symptoms of gastroparesis include early satiety, fullness, nausea, and vomiting. The symptoms may inhibit efforts at eating and recovery, but can be managed by limiting high-fiber foods, using liquid nutritional supplements, or using metoclopramide to increase emptying of food from the stomach. [195] Gastroparesis generally resolves when weight is regained.

Cardiac complications

Anorexia nervosa increases the risk of sudden cardiac death, though the precise cause is unknown. Cardiac complications include structural and functional changes to the heart. [196] Some of these cardiovascular changes are mild and are reversible with treatment, while others may be life-threatening. Cardiac complications can include arrhythmias, abnormally slow heart beat, low blood pressure, decreased size of the heart muscle, reduced heart volume, mitral valve prolapse, myocardial fibrosis, and pericardial effusion. [196]

Abnormalities in conduction and repolarization of the heart that can result from anorexia nervosa include QT prolongation, increased QT dispersion, conduction delays, and junctional escape rhythms. [196] Electrolyte abnormalities, particularly hypokalemia and hypomagnesemia, can cause anomalies in the electrical activity of the heart, and result in life-threatening arrhythmias. Hypokalemia most commonly results in patients with anorexia when restricting is accompanied by purging (induced vomiting or laxative use). Hypotension (low blood pressure) is common, and symptoms include fatigue and weakness. Orthostatic hypotension, a marked decrease in blood pressure when standing from a supine position, may also occur. Symptoms include lightheadedness upon standing, weakness, and cognitive impairment, and may result in fainting or near-fainting. [196] Orthostasis in anorexia nervosa indicates worsening cardiac function and may indicate a need for hospitalization. [196] Hypotension and orthostasis generally resolve upon recovery to a normal weight. The weight loss in anorexia nervosa also causes atrophy of cardiac muscle. This leads to decreased ability to pump blood, a reduction in the ability to sustain exercise, a diminished ability to increase blood pressure in response to exercise, and a subjective feeling of fatigue. [197]

Some individuals may also have a decrease in cardiac contractility. Cardiac complications can be life-threatening, but the heart muscle generally improves with weight gain, and the heart normalizes in size over weeks to months, with recovery. [197] Atrophy of the heart muscle is a marker of the severity of the disease, and while it is reversible with treatment and refeeding, it is possible that it may cause permanent, microscopic changes to the heart muscle that increase the risk of sudden cardiac death. [196] Individuals with anorexia nervosa may experience chest pain or palpitations; these can be a result of mitral valve prolapse. Mitral valve prolapse occurs because the size of the heart muscle decreases while the tissue of the mitral valve remains the same size. Studies have shown rates of mitral valve prolapse of around 20 percent in those with anorexia nervosa, while the rate in the general population is estimated at 2–4 percent. [198] It has been suggested that there is an association between mitral valve prolapse and sudden cardiac death, but it has not been proven to be causative, either in patients with anorexia nervosa or in the general population. [196]

Relapse

Rates of relapse after treatment range 30–72% over a period of 2–26 months, with a rate of approximately 50% in 12 months after weight restoration. [199] Relapse occurs in approximately a third of people in hospital, and is greatest in the first six to eighteen months after release from an institution. [200] BMI or measures of body fat and leptin levels at discharge were the strongest predictors of relapse, as well as signs of eating psychopathology at discharge. [199] Duration of illness, age, severity, the proportion of AN binge-purge subtype, and presence of comorbidities are also contributing factors.

Epidemiology

Anorexia is estimated to occur in 0.9% to 4.3% of women and 0.2% to 0.3% of men in Western countries at some point in their life. [20] About 0.4% of young females are affected in a given year and it is estimated to occur three to ten times less commonly in males. [4] [20] [200] [201] Rates in most of the developing world are unclear. [4] Often it begins during the teen years or young adulthood. [1] Medical students are a high risk group, with an overall estimated prevalence of 10.4% globally. [202]

The lifetime rate of atypical anorexia nervosa, a form of ED-NOS in which the person loses a significant amount of weight and is at risk for serious medical complications despite having a higher body-mass index, is much higher, at 5–12%. [203] Additionally, a UCSF study showed severity of illness is independent of current BMI, and "patients with large, rapid, or long-duration of weight loss were more severely ill regardless of their current weight." [204]

While anorexia became more commonly diagnosed during the 20th century it is unclear if this was due to an increase in its frequency or simply better diagnosis. [3] Most studies show that since at least 1970 the incidence of AN in adult women is fairly constant, while there is some indication that the incidence may have been increasing for girls aged between 14 and 20. [20]

Underrepresentation

In non-Westernized countries, including those in Africa (excluding South Africa), eating disorders are less frequently reported and studied compared to Western countries, [205] with available data mostly limited to case reports and isolated studies rather than prevalence investigations. Theories to explain these lower rates of eating disorders, lower reporting, and lower research rates in these countries include the attention to effects of westernisation and culture change on the prevalence of anorexia. [206] [ clarification needed ]

Male and female athletes are often overlooked as anorexic. [207] Research emphasizes the importance to take athletes' diet, weight and symptoms into account when diagnosing anorexia, instead of just looking at weight and BMI. For athletes, ritualized activities such as weigh-ins place emphasis on gaining and losing large amounts of weight, which may promote the development of eating disorders among them. [208] While women use diet pills, which is an indicator of unhealthy behavior and an eating disorder, men use steroids, which contextualizes the beauty ideals for genders. [62] In a Canadian study, 4% of boys in grade nine used anabolic steroids. [62] Anorexic men are sometimes referred to as manorexic. [209]

Moreover, some individuals, particularly men, who exhibit symptoms of anorexia may not meet the BMI criteria outlined in the DSM-IV due to higher muscle weight and lower fat content. [207] Consequently, a subclinical diagnosis, such as Eating Disorder Not Otherwise Specified (ED-NOS) in DSM-IV or Other Specified Feeding or Eating Disorder/Unspecified Feeding or Eating Disorder in DSM-5, is often made instead though there is no significant difference. [210]

Elderly

An increasing trend of anorexia among the elderly, termed "Anorexia of Aging," [211] is observed, characterized by behaviors similar to those seen in typical anorexia nervosa but often accompanied by excessive laxative use. [211] Most geriatric anorexia patients limit their food intake to dairy or grains, whereas an adolescent anorexic has a more general limitation. [211]

This eating disorder that affects older adults has two types – early onset and late onset. [211] Early onset refers to a recurrence of anorexia in late life in an individual who experienced the disease during their youth. [211] Late onset describes instances where the eating disorder begins for the first time late in life. [211]

The stimulus for anorexia in elderly patients is typically a loss of control over their lives, which can be brought on by many events, including moving into an assisted living facility. [212] This is also a time when most older individuals experience a rise in conflict with family members, such as limitations on driving or limitations on personal freedom, which increases the likelihood of an issue with anorexia. [212] There can be physical issues in the elderly that leads to anorexia of aging, including a decline in chewing ability, a decline in taste and smell, and a decrease in appetite. [213] Psychological reasons for the elderly to develop anorexia can include depression and bereavement, and even an indirect attempt at suicide. [213] There are also common comorbid psychiatric conditions with aging anorexics, including major depression, anxiety disorder, obsessive compulsive disorder, bipolar disorder, schizophrenia, and dementia. [214]

The signs and symptoms that go along with anorexia of aging are similar to what is observed in adolescent anorexia, including sudden weight loss, unexplained hair loss or dental problems, and a desire to eat alone. [212]

There are also several medical conditions that can result from anorexia in the elderly. An increased risk of illness and death can be a result of anorexia. [213] There is also a decline in muscle and bone mass as a result of a reduction in protein intake during anorexia. [213] Another result of anorexia in the aging population is irreparable damage to kidneys, heart or colon and an imbalance of electrolytes. [215]

Many assessments are available to diagnose anorexia in the aging community. These assessments include the Simplified Nutritional Assessment Questionnaire (SNAQ) [216] and Functional Assessment of Anorexia/Cachexia Therapy (FAACT). [217] [211] Specific to the geriatric populace, the interRAI system [218] identifies detrimental conditions in assisted living facilities and nursing homes. [211] Even a simple screening for nutritional insufficiencies such as low levels of important vitamins, can help to identify someone who has anorexia of aging. [211]

Anorexia in the elderly should be identified by the retirement communities but is often overlooked, [212] especially in patients with dementia. [215] Some studies report that malnutrition is prevalent in nursing homes, with up to 58% of residents suffering from it, which can lead to the difficulty of identifying anorexia. [215] One of the challenges with assisted living facilities is that they often serve bland, monotonous food, which lessens residents' desire to eat. [215]

The treatment for anorexia of aging is undifferentiated as anorexia for any other age group. Some of the treatment options include outpatient and inpatient facilities, antidepressant medication and behavioral therapy such as meal observation and discussing eating habits. [214]

History

Two images of an anorexic woman published in 1900 in "Nouvelle Iconographie de la Salpetriere". The case was titled "Un cas d'anorexie hysterique" (A case of hysteric anorexia). Anorexia case-1900-Nouvelle icononographie de la Salpetriere.jpg
Two images of an anorexic woman published in 1900 in "Nouvelle Iconographie de la Salpêtrière". The case was titled "Un cas d'anorexie hysterique" (A case of hysteric anorexia).

The history of anorexia nervosa begins with descriptions of religious fasting dating from the Hellenistic era [219] and continuing into the medieval period. The medieval practice of self-starvation by women, including some young women, in the name of religious piety and purity also concerns anorexia nervosa; it is sometimes referred to as anorexia mirabilis. [220] [221] The earliest medical descriptions of anorexic illnesses are generally credited to English physician Richard Morton in 1689. [219] Case descriptions fitting anorexic illnesses continued throughout the 17th, 18th, and 19th centuries. [222]

Etymologically, anorexia is a term of Greek origin: an- (ἀν-, prefix denoting negation) and orexis (ὄρεξις, "appetite"), translating literally to "a loss of appetite". In and of itself, this term does not have a harmful connotation, e.g., exercise-induced anorexia simply means that hunger is naturally suppressed during and after sufficiently intense exercise sessions. [223] It is the adjective nervosa that indicates the functional and non-organic nature of the disorder, but this adjective is also often omitted when the context is clear. Despite the literal translation of anorexia, the feeling of hunger in anorexia nervosa is frequently present and the pathological control of this instinct is a source of satisfaction for the patients. [224]

The term "anorexia nervosa" was coined in 1873 by Sir William Gull, one of Queen Victoria's personal physicians. [225] Gull published a seminal paper providing a number of detailed case descriptions of patients with anorexia nervosa. [222] In the same year, French physician Ernest-Charles Lasègue similarly published details of a number of cases in a paper entitled De l'Anorexie hystérique. [226]

In the late 19th century anorexia nervosa became widely accepted by the medical profession as a recognized condition. Awareness of the condition was largely limited to the medical profession until the latter part of the 20th century, when German-American psychoanalyst Hilde Bruch published The Golden Cage: the Enigma of Anorexia Nervosa in 1978. Despite major advances in neuroscience, [227] Bruch's theories tend to dominate popular thinking. A further important event was the death of the popular singer and drummer Karen Carpenter in 1983, which prompted widespread ongoing media coverage of eating disorders. [228]

See also

Related Research Articles

An eating disorder is a mental disorder defined by abnormal eating behaviors that adversely affect a person's physical or mental health. These behaviors include eating either too much or too little. Types of eating disorders include binge eating disorder, where the patient keeps eating large amounts in a short period of time typically while not being hungry; anorexia nervosa, where the person has an intense fear of gaining weight and restricts food or overexercises to manage this fear; bulimia nervosa, where individuals eat a large quantity (binging) then try to rid themselves of the food (purging); pica, where the patient eats non-food items; rumination syndrome, where the patient regurgitates undigested or minimally digested food; avoidant/restrictive food intake disorder (ARFID), where people have a reduced or selective food intake due to some psychological reasons; and a group of other specified feeding or eating disorders. Anxiety disorders, depression and substance abuse are common among people with eating disorders. These disorders do not include obesity. People often experience comorbidity between an eating disorder and OCD. It is estimated 20–60% of patients with an ED have a history of OCD.

<span class="mw-page-title-main">Bulimia nervosa</span> Type of eating disorder

Bulimia nervosa, also known simply as bulimia, is an eating disorder characterized by binge eating, followed by purging or fasting, as well as excessive concern with body shape and weight. This activity aims to expel the body of calories eaten from the binging phase of the process. Binge eating refers to eating a large amount of food in a short amount of time. Purging refers to the attempts to get rid of the food consumed. This may be done by vomiting or taking laxatives.

Orthorexia nervosa is a proposed eating disorder characterized by an excessive preoccupation with eating healthy food. The term was introduced in 1997 by American physician Steven Bratman, who suggested that some people's dietary restrictions intended to promote health may paradoxically lead to unhealthy consequences, such as social isolation, anxiety, loss of ability to eat in a natural, intuitive manner, reduced interest in the full range of other healthy human activities, and, in rare cases, severe malnutrition or even death.

<span class="mw-page-title-main">Appetite</span> Desire to eat food

Appetite is the desire to eat food items, usually due to hunger. Appealing foods can stimulate appetite even when hunger is absent, although appetite can be greatly reduced by satiety. Appetite exists in all higher life-forms, and serves to regulate adequate energy intake to maintain metabolic needs. It is regulated by a close interplay between the digestive tract, adipose tissue and the brain. Appetite has a relationship with every individual's behavior. Appetitive behaviour also known as approach behaviour, and consummatory behaviour, are the only processes that involve energy intake, whereas all other behaviours affect the release of energy. When stressed, appetite levels may increase and result in an increase of food intake. Decreased desire to eat is termed anorexia, while polyphagia is increased eating. Dysregulation of appetite contributes to ARFID, anorexia nervosa, bulimia nervosa, cachexia, overeating, and binge eating disorder.

Binge eating disorder (BED) is an eating disorder characterized by frequent and recurrent binge eating episodes with associated negative psychological and social problems, but without the compensatory behaviors common to bulimia nervosa, OSFED, or the binge-purge subtype of anorexia nervosa.

Binge eating is a pattern of disordered eating which consists of episodes of uncontrollable eating. It is a common symptom of eating disorders such as binge eating disorder and bulimia nervosa. During such binges, a person rapidly consumes an excessive quantity of food. A diagnosis of binge eating is associated with feelings of loss of control. Binge eating disorder is also linked with being overweight and obesity.

<span class="mw-page-title-main">Rumination syndrome</span> Medical condition

Rumination syndrome, or merycism, is a chronic motility disorder characterized by effortless regurgitation of most meals following consumption, due to the involuntary contraction of the muscles around the abdomen. There is no retching, nausea, heartburn, odour, or abdominal pain associated with the regurgitation as there is with typical vomiting, and the regurgitated food is undigested. The disorder has been historically documented as affecting only infants, young children, and people with cognitive disabilities . It is increasingly being diagnosed in a greater number of otherwise healthy adolescents and adults, though there is a lack of awareness of the condition by doctors, patients, and the general public.

Night eating syndrome (NES) is classified as an Other Specified Feeding or Eating Disorder (OSFED) under the DSM-5, involving recurrent episodes of night eating after awakening from sleep or after the evening meal. There is awareness and recall of the eating, a key characteristic that differentiates the disorder from Sleep-Related Eating Disorder (SRED). Although there is some degree of comorbidity with binge eating disorder (BED), it differs from binge eating in that the amount of food consumed in the night is not necessarily objectively large nor is a loss of control over food intake required. The syndrome causes significant distress or functional impairment and cannot be better explained by external influences such as changes in the sleep-wake cycle, social norms, substance use, medication, or another mental or medical disorder.

The Eating Attitudes Test, created by David Garner, is a widely used 26-item, standardized self-reported questionnaire of symptoms and concerns characteristic of eating disorders. The EAT is useful in assessing "eating disorder risk" in high school, college and other special risk samples such as athletes. EAT has been extremely effective in screening for anorexia nervosa in many populations.

Avoidant restrictive food intake disorder (ARFID) is a feeding or eating disorder in which individuals significantly limit the volume or variety of foods they consume, causing malnutrition, weight loss, and/or psychosocial problems. Unlike eating disorders such as anorexia nervosa and bulimia, body image disturbance is not a root cause. Individuals with ARFID may have trouble eating due to the sensory characteristics of food ; executive function disregulation; fears of choking or vomiting; low appetite; or a combination of these factors. While ARFID is most often associated with low weight, ARFID occurs across the whole weight spectrum.

Diabulimia, also known as ED-DMT1 in the US or T1ED in the UK, is an eating disorder in which people with type 1 diabetes deliberately give themselves less insulin than they need or stop taking it altogether for the purpose of weight loss. Diabulimia is not recognized as a formal psychiatric diagnosis in the DSM-5. Because of this, some in the medical or psychiatric communities use the phrases "disturbed eating behavior" or "disordered eating behavior" and disordered eating (DE) are quite common in medical and psychiatric literature addressing patients who have type 1 diabetes and manipulate insulin doses to control weight along with exhibiting bulimic behavior.

Purging disorder is an eating disorder characterized by the DSM-5 as self-induced vomiting, or misuse of laxatives, diuretics, or enemas to forcefully evacuate matter from the body. Purging disorder differs from bulimia nervosa (BN) because individuals do not consume a large amount of food before they purge. In current diagnostic systems, purging disorder is a form of other specified feeding or eating disorder. Research indicates that purging disorder, while not rare, is not as commonly found as anorexia nervosa or bulimia nervosa. This syndrome is associated with clinically significant levels of distress, and that it appears to be distinct from bulimia nervosa on measures of hunger and ability to control food intake. Some of the signs of purging disorder are frequent trips to the bathroom directly after a meal, frequent use of laxatives, and obsession over one's appearance and weight. Other signs include swollen cheeks, popped blood vessels in the eyes, and clear teeth which are all signs of excessive vomiting.

Maudsley family therapy, also known as family-based treatment or Maudsley approach, is a family therapy for the treatment of anorexia nervosa devised by Christopher Dare and colleagues at the Maudsley Hospital in London. A comparison of family to individual therapy was conducted with eighty anorexia patients. The study showed family therapy to be the more effective approach in patients under 18 and within 3 years of the onset of their illness. Subsequent research confirmed the efficacy of family-based treatment for teens with anorexia nervosa. Family-based treatment has been adapted for bulimia nervosa and showed promising results in a randomized controlled trial comparing it to supportive individual therapy.

The differential diagnoses of anorexia nervosa (AN) includes various types of medical and psychological conditions, which may be misdiagnosed as AN. In some cases, these conditions may be comorbid with AN because the misdiagnosis of AN is not uncommon. For example, a case of achalasia was misdiagnosed as AN and the patient spent two months confined to a psychiatric hospital. A reason for the differential diagnoses that surround AN arise mainly because, like other disorders, it is primarily, albeit defensively and adaptive for, the individual concerned. Anorexia Nervosa is a psychological disorder characterized by extremely reduced intake of food. People with anorexia nervosa tend to have a low self-image and an inaccurate perception of their body.

Cognitive behavioral therapy (CBT) is derived from both the cognitive and behavioral schools of psychology and focuses on the alteration of thoughts and actions with the goal of treating various disorders. The cognitive behavioral treatment of eating disorders emphasizes on the minimization of negative thoughts about body image and the act of eating, and attempts to alter negative and harmful behaviors that are involved in and perpetuate eating disorders. It also encourages the ability to tolerate negative thoughts and feelings as well as the ability to think about food and body perception in a multi-dimensional way. The emphasis is not only placed on altering cognition, but also on tangible practices like making goals and being rewarded for meeting those goals. CBT is a "time-limited and focused approach" which means that it is important for the patients of this type of therapy to have particular issues that they want to address when they begin treatment. CBT has also proven to be one of the most effective treatments for eating disorders.

Chew and spit is a compensatory behavior associated with several eating disorders that involves chewing food and spitting it out before swallowing, often as an attempt to avoid ingesting unwanted or unnecessary calories. CS can be used as a way to taste food viewed as “forbidden” or unhealthy. Individuals who partake in CS typically have an increased desire for thinness, increased loss of control (LOC) and body dissatisfaction. CS can replace vomiting and/or binging behaviors, or serve as an additional behavior to many eating disorders.

Paul E. Garfinkel is a Canadian psychiatrist, researcher and an academic leader. He is a professor at the University of Toronto and a staff psychiatrist at Centre for Addiction and Mental Health (CAMH).

Body image disturbance (BID) is a common symptom in patients with eating disorders and is characterized by an altered perception of one's own body.

Atypical anorexia nervosa is an eating disorder in which individuals meet all the qualifications for anorexia nervosa, including a body image disturbance and a history of restrictive eating and weight loss, except that they are not currently underweight. Atypical anorexia qualifies as a mental health disorder in the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), under the category Other Specified Feeding and Eating Disorders (OSFED). The characteristics of people with atypical anorexia generally do not differ significantly from anorexia nervosa patients except for their current weight.

Body checking is a compulsive behaviour related but not exclusive to various forms of body dysmorphic disorders. It involves frequently collecting various information about one’s own body in terms of size, shape, appearance or weight. Frequent expressions of this form of behaviour entails for example mirror checking, trying to feel one’s own bones, pinching the abdomen, frequent body weight measurement and comparing your own body to that of others. Studies have shown that an increased rate of body checking correlates with an overall increased dissatisfaction with the own body.

References

  1. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 "What are Eating Disorders?". NIMH. Archived from the original on 23 May 2015. Retrieved 24 May 2015.
  2. "Anorexia Nervosa". My.clevelandclinic.org. Retrieved 9 June 2022.
  3. 1 2 3 4 5 6 7 Attia E (2010). "Anorexia nervosa: current status and future directions". Annual Review of Medicine. 61 (1): 425–435. doi:10.1146/annurev.med.050208.200745. PMID   19719398.
  4. 1 2 3 4 5 6 7 8 9 10 11 12 Diagnostic and statistical manual of mental disorders : DSM-5 (5 ed.). Washington: American Psychiatric Publishing. 2013. pp.  338–345. ISBN   978-0-89042-555-8.
  5. 1 2 Arcelus J, Witcomb GL, Mitchell A (March 2014). "Prevalence of eating disorders amongst dancers: a systemic review and meta-analysis". European Eating Disorders Review. 22 (2): 92–101. doi:10.1002/erv.2271. PMID   24277724.
  6. Parker R, Sharma A (2008). General Medicine. Elsevier Health Sciences. p. 56. ISBN   978-0-7234-3461-0.
  7. First MB (19 November 2013). DSM-5 Handbook of Differential Diagnosis. American Psychiatric Pub. ISBN   978-1-58562-462-1 via Google Books.
  8. 1 2 3 4 5 6 7 8 "Feeding and eating disorders" (PDF). American Psychiatric Publishing. 2013. Archived from the original (PDF) on 1 May 2015. Retrieved 9 April 2015.
  9. 1 2 3 4 5 6 7 Espie J, Eisler I (2015). "Focus on anorexia nervosa: modern psychological treatment and guidelines for the adolescent patient". Adolescent Health, Medicine and Therapeutics. 6: 9–16. doi: 10.2147/AHMT.S70300 . PMC   4316908 . PMID   25678834.
  10. Vos T, Allen C, Arora M, Barber RM, Bhutta ZA, Brown A, et al. (GBD 2015 Disease and Injury Incidence and Prevalence Collaborators) (October 2016). "Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015". Lancet. 388 (10053): 1545–1602. doi:10.1016/S0140-6736(16)31678-6. ISSN   0140-6736. PMC   5055577 . PMID   27733282.
  11. Wang H, Naghavi M, Allen C, Barber RM, Bhutta ZA, Carter A, et al. (GBD 2015 Mortality and Causes of Death Collaborators) (October 2016). "Global, regional, and national life expectancy, all-cause mortality, and cause-specific mortality for 249 causes of death, 1980–2015: a systematic analysis for the Global Burden of Disease Study 2015". Lancet. 388 (10053): 1459–1544. doi:10.1016/S0140-6736(16)31012-1. PMC   5388903 . PMID   27733281.
  12. 1 2 3 Treasure J, Zipfel S, Micali N, Wade T, Stice E, Claudino A, et al. (November 2015). "Anorexia nervosa". Nature Reviews. Disease Primers. 1: 15074. doi:10.1038/nrdp.2015.74. PMID   27189821. S2CID   21580134.
  13. 1 2 Artoni P, Chierici ML, Arnone F, Cigarini C, De Bernardis E, Galeazzi GM, et al. (March 2021). "Body perception treatment, a possible way to treat body image disturbance in eating disorders: a case-control efficacy study". Eating and Weight Disorders. 26 (2): 499–514. doi:10.1007/s40519-020-00875-x. PMID   32124409. S2CID   211728899.
  14. 1 2 Kodua M, Mackenzie JM, Smyth N (December 2020). "Nursing assistants' experiences of administering manual restraint for compulsory nasogastric feeding of young persons with anorexia nervosa". International Journal of Mental Health Nursing. 29 (6): 1181–1191. doi:10.1111/inm.12758. PMID   32578949. S2CID   220046454.
  15. "Proxy definition and meaning". Collins English Dictionary. Retrieved 2 October 2020.
  16. "Force-Feeding of Anorexic Patients and the Right to Die" (PDF). Archived from the original (PDF) on 23 November 2020. Retrieved 2 October 2020.
  17. Sudi K, Öttl K, Payerl D, Baumgartl P, Tauschmann K, Müller W (2004). "Anorexia athletica". Nutrition. 20 (7–8): 657–661. doi:10.1016/j.nut.2004.04.019. PMID   15212748.
  18. Hay P (July 2013). "A systematic review of evidence for psychological treatments in eating disorders: 2005–2012". The International Journal of Eating Disorders. 46 (5): 462–469. doi:10.1002/eat.22103. PMID   23658093.
  19. 1 2 3 "Eating Disorders: Core Interventions in the Treatment and Management of Anorexia Nervosa, Bulimia Nervosa and Related Eating Disorders" (PDF). 2004. p. 103. PMID   23346610.
  20. 1 2 3 4 5 6 Smink FR, van Hoeken D, Hoek HW (August 2012). "Epidemiology of eating disorders: incidence, prevalence and mortality rates". Current Psychiatry Reports. 14 (4): 406–414. doi:10.1007/s11920-012-0282-y. PMC   3409365 . PMID   22644309.
  21. Murray CJ, Barber RM, Foreman KJ, Ozgoren AA, Abd-Allah F, Abera SF, et al. (GBD 2013 Mortality and Causes of Death Collaborators) (January 2015). "Global, regional, and national age-sex specific all-cause and cause-specific mortality for 240 causes of death, 1990–2013: a systematic analysis for the Global Burden of Disease Study 2013". Lancet. 385 (9963): 117–171. doi:10.1016/S0140-6736(14)61682-2. PMC   4340604 . PMID   25530442.
  22. 1 2 Surgenor LJ, Maguire S (2013). "Assessment of anorexia nervosa: an overview of universal issues and contextual challenges". Journal of Eating Disorders. 1 (1): 29. doi: 10.1186/2050-2974-1-29 . PMC   4081667 . PMID   24999408.
  23. 1 2 3 4 Strumia R (September 2009). "Skin signs in anorexia nervosa". Dermato-Endocrinology. 1 (5): 268–270. doi:10.4161/derm.1.5.10193. PMC   2836432 . PMID   20808514.
  24. 1 2 3 4 Miller KK (September 2013). "Endocrine effects of anorexia nervosa". Endocrinology and Metabolism Clinics of North America. 42 (3): 515–528. doi:10.1016/j.ecl.2013.05.007. PMC   3769686 . PMID   24011884.
  25. Walsh JM, Wheat ME, Freund K (August 2000). "Detection, evaluation, and treatment of eating disorders the role of the primary care physician". Journal of General Internal Medicine. 15 (8): 577–590. doi:10.1046/j.1525-1497.2000.02439.x. PMC   1495575 . PMID   10940151.
  26. Stargrove MB, Treasure J, McKee DL (2008). Herb, Nutrient, and Drug Interactions: Clinical Implications and Therapeutic Strategies. Elsevier Health Sciences. ISBN   978-0-323-02964-3 . Retrieved 9 April 2015.
  27. American Psychiatric Association (22 May 2013). Diagnostic and Statistical Manual of Mental Disorders (5th ed.). American Psychiatric Association. p. 339. doi:10.1176/appi.books.9780890425596. ISBN   978-0-89042-555-8 . Retrieved 29 February 2024.
  28. Poyastro Pinheiro A, Thornton LM, Plotonicov KH, Tozzi F, Klump KL, Berrettini WH, et al. (July 2007). "Patterns of menstrual disturbance in eating disorders". The International Journal of Eating Disorders. 40 (5): 424–434. doi:10.1002/eat.20388. ISSN   0276-3478. PMID   17497704.
  29. Mehler PS, Brown C (31 March 2015). "Anorexia nervosa – medical complications". Journal of Eating Disorders. 3 (1): 11. doi: 10.1186/s40337-015-0040-8 . ISSN   2050-2974. PMC   4381361 . PMID   25834735.
  30. Smith LL (6 August 2021). "The Central Role of Hypothermia and Hyperactivity in Anorexia Nervosa: A Hypothesis". Frontiers in Behavioral Neuroscience. 15. doi: 10.3389/fnbeh.2021.700645 . ISSN   1662-5153. PMC   8377352 . PMID   34421554.
  31. "Anorexia Nervosa". National Association of Anorexia Nervosa and Associated Disorders. Archived from the original on 13 April 2014. Retrieved 15 April 2014.
  32. Hedrick T (August 2022). "The Overlap Between Eating Disorders and Gastrointestinal Disorders" (PDF). Nutrition issues in Gastroenterology. University of Virginia. Archived from the original (PDF) on 8 February 2024.
  33. 1 2 3 Nolen-Hoeksema S (2013). Abnormal Psychology. New York: McGraw Hill. pp. 339–41. ISBN   978-0-07-803538-8.
  34. Walsh JM, Wheat ME, Freund K (August 2000). "Detection, evaluation, and treatment of eating disorders the role of the primary care physician". Journal of General Internal Medicine. 15 (8): 577–590. doi:10.1046/j.1525-1497.2000.02439.x. PMC   1495575 . PMID   10940151.
  35. Walsh BT (May 2013). "The Enigmatic Persistence of Anorexia Nervosa". American Journal of Psychiatry. 170 (5): 477–484. doi:10.1176/appi.ajp.2012.12081074. ISSN   0002-953X. PMC   4095887 . PMID   23429750.
  36. Bora E, Köse S (August 2016). "Meta-analysis of theory of mind in anorexia nervosa and bulimia nervosa: A specific İmpairment of cognitive perspective taking in anorexia nervosa?". The International Journal of Eating Disorders. 49 (8): 739–740. doi:10.1002/eat.22572. hdl: 11343/291969 . PMID   27425037.
  37. "Anorexia nervosa". National Eating Disorders Collaboration (NEDC). 23 August 2017. Retrieved 19 September 2022.
  38. 1 2 Marzola E, Nasser JA, Hashim SA, Shih PA, Kaye WH (November 2013). "Nutritional rehabilitation in anorexia nervosa: review of the literature and implications for treatment". BMC Psychiatry. 13 (1): 290. doi: 10.1186/1471-244X-13-290 . PMC   3829207 . PMID   24200367.
  39. Robinson PH (2006). Community treatment of eating disorders. Chichester: John Wiley & Sons. p. 66. ISBN   978-0-470-01676-3.
  40. Haller E (December 1992). "Eating disorders. A review and update". The Western Journal of Medicine. 157 (6): 658–662. PMC   1022101 . PMID   1475950.
  41. Khalsa SS, Adolphs R, Cameron OG, Critchley HD, Davenport PW, Feinstein JS, et al. (June 2018). "Interoception and Mental Health: A Roadmap". Biological Psychiatry. Cognitive Neuroscience and Neuroimaging. 3 (6): 501–513. doi:10.1016/j.bpsc.2017.12.004. PMC   6054486 . PMID   29884281.
  42. 1 2 Badoud D, Tsakiris M (June 2017). "From the body's viscera to the body's image: Is there a link between interoception and body image concerns?". Neuroscience and Biobehavioral Reviews. 77: 237–246. doi:10.1016/j.neubiorev.2017.03.017. PMID   28377099. S2CID   768206.
  43. 1 2 3 Khalsa SS, Lapidus RC (2016). "Can Interoception Improve the Pragmatic Search for Biomarkers in Psychiatry?". Frontiers in Psychiatry. 7: 121. doi: 10.3389/fpsyt.2016.00121 . PMC   4958623 . PMID   27504098.
  44. 1 2 3 4 5 Boswell JF, Anderson LM, Anderson DA (June 2015). "Integration of Interoceptive Exposure in Eating Disorder Treatment". Clinical Psychology: Science and Practice. 22 (2): 194–210. doi:10.1111/cpsp.12103.
  45. Kasperek-Zimowska BJ, Zimowski JG, Biernacka K, Kucharska-Pietura K, Rybakowski F (2014). "Impaired social cognition processes in Asperger syndrome and anorexia nervosa. In search for endophenotypes of social cognition". Psychiatria Polska. 50 (3): 533–542. doi: 10.12740/PP/OnlineFirst/33485 . PMID   27556112.
  46. Strober M, Freeman R, Lampert C, Diamond J (November 2007). "The association of anxiety disorders and obsessive compulsive personality disorder with anorexia nervosa: evidence from a family study with discussion of nosological and neurodevelopmental implications". The International Journal of Eating Disorders. 40 (S3): S46–S51. doi: 10.1002/eat.20429 . PMID   17610248.
  47. Brand-Gothelf A, Leor S, Apter A, Fennig S (October 2014). "The impact of comorbid depressive and anxiety disorders on severity of anorexia nervosa in adolescent girls". The Journal of Nervous and Mental Disease. 202 (10): 759–762. doi:10.1097/NMD.0000000000000194. PMID   25265267. S2CID   6023688.
  48. Godier LR, Park RJ (2014). "Compulsivity in anorexia nervosa: a transdiagnostic concept". Frontiers in Psychology. 5: 778. doi: 10.3389/fpsyg.2014.00778 . PMC   4101893 . PMID   25101036.
  49. Halmi KA, Tozzi F, Thornton LM, Crow S, Fichter MM, Kaplan AS, et al. (December 2005). "The relation among perfectionism, obsessive-compulsive personality disorder and obsessive-compulsive disorder in individuals with eating disorders". The International Journal of Eating Disorders. 38 (4): 371–374. doi: 10.1002/eat.20190 . PMID   16231356.
  50. Crane AM, Roberts ME, Treasure J (November 2007). "Are obsessive-compulsive personality traits associated with a poor outcome in anorexia nervosa? A systematic review of randomized controlled trials and naturalistic outcome studies". The International Journal of Eating Disorders. 40 (7): 581–588. doi: 10.1002/eat.20419 . PMID   17607713.
  51. Gárriz M, Andrés-Perpiñá S, Plana MT, Flamarique I, Romero S, Julià L, et al. (March 2021). "Personality disorder traits, obsessive ideation and perfectionism 20 years after adolescent-onset anorexia nervosa: a recovered study". Eating and Weight Disorders. 26 (2): 667–677. doi:10.1007/s40519-020-00906-7. PMID   32350776. S2CID   216649851. However, prospective studies are still scarce and the results from current literature regarding causal connections between AN and personality are unavailable.
  52. Casper RC (1998). "Depression and eating disorders". Depression and Anxiety. 8 (Suppl 1): 96–104. doi: 10.1002/(SICI)1520-6394(1998)8:1+<96::AID-DA15>3.0.CO;2-4 . PMID   9809221. S2CID   36772859.
  53. Zernig G, Saria A, Kurz M, O'Malley S (24 March 2000). Handbook of Alcoholism. CRC Press. p.  293. ISBN   978-1-4200-3696-1.
  54. Sansone RA, Levitt JL (21 August 2013). Personality Disorders and Eating Disorders: Exploring the Frontier. Routledge. p.  28. ISBN   978-1-135-44280-4.
  55. Halmi KA (November 2013). "Perplexities of treatment resistance in eating disorders". BMC Psychiatry. 13: 292. doi: 10.1186/1471-244X-13-292 . PMC   3829659 . PMID   24199597.
  56. Swinbourne JM, Touyz SW (July 2007). "The co-morbidity of eating disorders and anxiety disorders: a review". European Eating Disorders Review. 15 (4): 253–274. doi: 10.1002/erv.784 . PMID   17676696.
  57. Cortese S, Bernardina BD, Mouren MC (September 2007). "Attention-deficit/hyperactivity disorder (ADHD) and binge eating". Nutrition Reviews. 65 (9): 404–411. doi: 10.1111/j.1753-4887.2007.tb00318.x . PMID   17958207.
  58. Wilhelm S, Phillips KA, Steketee G (18 December 2012). Cognitive-Behavioral Therapy for Body Dysmorphic Disorder: A Treatment Manual. Guilford Press. p.  270. ISBN   978-1-4625-0790-0.
  59. 1 2 Berkman ND, Bulik CM, Brownley KA, Lohr KN, Sedway JA, Rooks A, et al. (April 2006). "Management of eating disorders" (PDF). Evidence Report/Technology Assessment (135): 1–166. PMC   4780981 . PMID   17628126. Archived (PDF) from the original on 22 December 2014.
  60. Huke V, Turk J, Saeidi S, Kent A, Morgan JF (September 2013). "Autism spectrum disorders in eating disorder populations: a systematic review". European Eating Disorders Review. 21 (5): 345–351. doi:10.1002/erv.2244. PMID   23900859.
  61. 1 2 Zucker NL, Losh M, Bulik CM, LaBar KS, Piven J, Pelphrey KA (November 2007). "Anorexia nervosa and autism spectrum disorders: guided investigation of social cognitive endophenotypes" (PDF). Psychological Bulletin. 133 (6): 976–1006. doi:10.1037/0033-2909.133.6.976. PMID   17967091. Archived (PDF) from the original on 20 April 2010.
  62. 1 2 3 4 5 6 Rikani AA, Choudhry Z, Choudhry AM, Ikram H, Asghar MW, Kajal D, et al. (October 2013). "A critique of the literature on etiology of eating disorders". Annals of Neurosciences. 20 (4): 157–161. doi:10.5214/ans.0972.7531.200409. PMC   4117136 . PMID   25206042.
  63. Thornton LM, Mazzeo SE, Bulik CM (2011). "The heritability of eating disorders: methods and current findings". Behavioral Neurobiology of Eating Disorders. Current Topics in Behavioral Neurosciences. Vol. 6. pp. 141–56. doi:10.1007/7854_2010_91. ISBN   978-3-642-15130-9. PMC   3599773 . PMID   21243474.
  64. Hildebrandt T, Downey A (4 July 2013). "The Neurobiology of Eating Disorders". In Charney D, Sklar P, Buxbaum J, Nestler E (eds.). Neurobiology of Mental Illness (4th ed.). Oxford University Press. ISBN   978-0-19-993495-9.
  65. Rask-Andersen M, Olszewski PK, Levine AS, Schiöth HB (March 2010). "Molecular mechanisms underlying anorexia nervosa: focus on human gene association studies and systems controlling food intake". Brain Research Reviews. 62 (2): 147–164. doi:10.1016/j.brainresrev.2009.10.007. PMID   19931559. S2CID   37635456.
  66. Pjetri E, Schmidt U, Kas MJ, Campbell IC (July 2012). "Epigenetics and eating disorders". Current Opinion in Clinical Nutrition and Metabolic Care. 15 (4): 330–335. doi:10.1097/MCO.0b013e3283546fd3. PMID   22617563. S2CID   27183934.
  67. Hübel C, Marzi SJ, Breen G, Bulik CM (June 2019). "Epigenetics in eating disorders: a systematic review". Molecular Psychiatry. 24 (6): 901–915. doi:10.1038/s41380-018-0254-7. PMC   6544542 . PMID   30353170.
  68. Watson HJ, Yilmaz Z, Thornton LM, Hübel C, Coleman JR, Gaspar HA, et al. (August 2019). "Genome-wide association study identifies eight risk loci and implicates metabo-psychiatric origins for anorexia nervosa". Nature Genetics. 51 (8): 1207–1214. doi:10.1038/s41588-019-0439-2. PMC   6779477 . PMID   31308545.
  69. Larsen JT, Bulik CM, Thornton LM, Koch SV, Petersen L (April 2021). "Prenatal and perinatal factors and risk of eating disorders". Psychological Medicine. 51 (5): 870–880. doi:10.1017/S0033291719003945. PMID   31910913. S2CID   210086516.
  70. Jones C, Pearce B, Barrera I, Mummert A (September 2017). "Fetal programming and eating disorder risk". Journal of Theoretical Biology. 428: 26–33. Bibcode:2017JThBi.428...26J. doi:10.1016/j.jtbi.2017.05.028. PMID   28571669.
  71. Favaro A, Tenconi E, Santonastaso P (January 2006). "Perinatal factors and the risk of developing anorexia nervosa and bulimia nervosa". Archives of General Psychiatry. 63 (1): 82–88. doi:10.1001/archpsyc.63.1.82. PMID   16389201. S2CID   45181444.
  72. Davis JF, Choi DL, Benoit SC (2011). "24. Orexigenic Hypothalamic Peptides Behavior and Feeding – 24.5 Orexin". In Preedy VR, Watson RR, Martin CR (eds.). Handbook of Behavior, Food and Nutrition. Springer. pp.  361–2. ISBN   978-0-387-92271-3.
  73. Smitka K, Papezova H, Vondra K, Hill M, Hainer V, Nedvidkova J (2013). "The role of "mixed" orexigenic and anorexigenic signals and autoantibodies reacting with appetite-regulating neuropeptides and peptides of the adipose tissue-gut-brain axis: relevance to food intake and nutritional status in patients with anorexia nervosa and bulimia nervosa". International Journal of Endocrinology. 2013: 483145. doi: 10.1155/2013/483145 . PMC   3782835 . PMID   24106499.
  74. 1 2 Satherley R, Howard R, Higgs S (January 2015). "Disordered eating practices in gastrointestinal disorders" (PDF). Appetite (Review). 84: 240–250. doi:10.1016/j.appet.2014.10.006. PMID   25312748. S2CID   25805182. Archived from the original (PDF) on 24 September 2019. Retrieved 4 July 2019.
  75. 1 2 Bern EM, O'Brien RF (August 2013). "Is it an eating disorder, gastrointestinal disorder, or both?". Current Opinion in Pediatrics (Review). 25 (4): 463–470. doi:10.1097/MOP.0b013e328362d1ad. PMID   23838835. S2CID   5417088. Several case reports brought attention to the association of anorexia nervosa and celiac disease.(...) Some patients present with the eating disorder prior to diagnosis of celiac disease and others developed anorexia nervosa after the diagnosis of celiac disease. Healthcare professionals should screen for celiac disease with eating disorder symptoms especially with gastrointestinal symptoms, weight loss, or growth failure.(...) Celiac disease patients may present with gastrointestinal symptoms such as diarrhea, steatorrhea, weight loss, vomiting, abdominal pain, anorexia, constipation, bloating, and distension due to malabsorption. Extraintestinal presentations include anemia, osteoporosis, dermatitis herpetiformis, short stature, delayed puberty, fatigue, aphthous stomatitis, elevated transaminases, neurologic problems, or dental enamel hypoplasia.(...) it has become clear that symptomatic and diagnosed celiac disease is the tip of the iceberg; the remaining 90% or more of children are asymptomatic and undiagnosed.
  76. Sainsbury K, Mullan B, Sharpe L (August 2013). "Reduced quality of life in coeliac disease is more strongly associated with depression than gastrointestinal symptoms". Journal of Psychosomatic Research. 75 (2): 135–141. doi:10.1016/j.jpsychores.2013.05.011. hdl: 20.500.11937/40065 . PMID   23915769.
  77. Tang TN, Toner BB, Stuckless N, Dion KL, Kaplan AS, Ali A (August 1998). "Features of eating disorders in patients with irritable bowel syndrome". Journal of Psychosomatic Research. 45 (2): 171–178. doi:10.1016/s0022-3999(97)00300-0. PMID   9753389.
  78. Leffler DA, Dennis M, Edwards George JB, Jamma S, Magge S, Cook EF, et al. (May 2009). "A simple validated gluten-free diet adherence survey for adults with celiac disease". Clinical Gastroenterology and Hepatology. 7 (5): 530–536, 536.e1–2. doi:10.1016/j.cgh.2008.12.032. PMID   19268725.
  79. Garcia J, Kimeldorf DJ, Koelling RA (July 1955). "Conditioned aversion to saccharin resulting from exposure to gamma radiation". Science. 122 (3160): 157–158. Bibcode:1955Sci...122..157G. doi:10.1126/science.122.3160.157. PMID   14396377. S2CID   30826975.
  80. Quick VM, Byrd-Bredbenner C, Neumark-Sztainer D (May 2013). "Chronic illness and disordered eating: a discussion of the literature". Advances in Nutrition (Review). 4 (3): 277–286. doi:10.3945/an.112.003608. PMC   3650496 . PMID   23674793.
  81. 1 2 Herpertz-Dahlmann B, Bühren K, Remschmidt H (June 2013). "Growing up is hard: mental disorders in adolescence". Deutsches Ärzteblatt International. 110 (25): 432–9, quiz 440. doi:10.3238/arztebl.2013.0432. PMC   3705204 . PMID   23840288.
  82. Chen D, Steele AD, Lindquist S, Guarente L (9 December 2005). "Increase in activity during calorie restriction requires Sirt1". Science. 310 (5754): 1641. doi:10.1126/science.1118357. ISSN   1095-9203. PMID   16339438.
  83. Zandian M, Ioakimidis I, Bergh C, Södersten P (September 2007). "Cause and treatment of anorexia nervosa". Physiology & Behavior. 92 (1–2): 283–290. doi:10.1016/j.physbeh.2007.05.052. PMID   17585973. S2CID   43620773.
  84. Thambirajah MS (2007). Case Studies in Child and Adolescent Mental Health. Radcliffe Publishing. p. 145. ISBN   978-1-85775-698-2. OCLC   84150452.
  85. 1 2 Kaye W (April 2008). "Neurobiology of anorexia and bulimia nervosa". Physiology & Behavior. 94 (1): 121–135. doi:10.1016/j.physbeh.2007.11.037. PMC   2601682 . PMID   18164737.
  86. Guisinger S (October 2003). "Adapted to flee famine: adding an evolutionary perspective on anorexia nervosa". Psychological Review. 110 (4): 745–761. doi:10.1037/0033-295X.110.4.745. ISSN   0033-295X. PMID   14599241.
  87. Guisinger S. "Adapted to Famine: An Evolutionary Approach to Understanding Eating Behaviors". Archived from the original on 22 June 2024.
  88. Wonderlich SA, Brewerton TD, Jocic Z, Dansky BS, Abbott DW (August 1997). "Relationship of childhood sexual abuse and eating disorders". Journal of the American Academy of Child and Adolescent Psychiatry. 36 (8): 1107–1115. doi:10.1097/00004583-199708000-00018. PMID   9256590.
  89. Connors ME, Morse W (January 1993). "Sexual abuse and eating disorders: a review". The International Journal of Eating Disorders. 13 (1): 1–11. doi:10.1002/1098-108x(199301)13:1<1::aid-eat2260130102>3.0.co;2-p. PMID   8477269.
  90. Worthen D (2001). P & G Pharmacy Handbook. Boca Raton, FL: Routledge. p. 65. ISBN   978-1-4822-9648-8.
  91. Ensminger AH (1983). Foods and Nutrition Encyclopedia (1st ed.). Clovis, California: Pegus Press. p. 423. ISBN   978-0-941218-05-4.
  92. Colman A (2015). A Dictionary of Psychology. OUP Oxford. p. 851. ISBN   978-0-19-105784-7.
  93. Rogers AI, Vanderveldt HS, Deshpande AR (2012). "Weight Loss". In Hawkey CJ, Bosch J, Richter JE, Garcia-Tsao G, Chan FK (eds.). Textbook of Clinical Gastroenterology and Hepatology (2nd ed.). John Wiley & Sons. p. 69. ISBN   978-1-118-32142-3.
  94. 1 2 "Factors That May Contribute to Eating Disorders". National Eating Disorders Association. Archived from the original on 3 March 2016. Retrieved 1 March 2016.
  95. Halmi KA, Sunday SR, Strober M, Kaplan A, Woodside DB, Fichter M, et al. (November 2000). "Perfectionism in anorexia nervosa: variation by clinical subtype, obsessionality, and pathological eating behavior". The American Journal of Psychiatry. 157 (11): 1799–1805. doi:10.1176/appi.ajp.157.11.1799. PMID   11058477.
  96. Anderluh MB, Tchanturia K, Rabe-Hesketh S, Treasure J (February 2003). "Childhood obsessive-compulsive personality traits in adult women with eating disorders: defining a broader eating disorder phenotype". The American Journal of Psychiatry. 160 (2): 242–247. doi:10.1176/appi.ajp.160.2.242. PMID   12562569.
  97. "Anorexia Nervosa". Mayo Clinic .
  98. Flett GL, Newby J, Hewitt PL, Persaud C (September 2011). "Perfectionistic automatic thoughts, trait perfectionism, and bulimic automatic thoughts in young women". Journal of Rational-Emotive & Cognitive-Behavior Therapy. 29 (3): 192–206. doi:10.1007/s10942-011-0135-3. S2CID   144731404.
  99. Garner DM, Bemis KM (June 1982). "A cognitive-behavioral approach to anorexia nervosa". Cognitive Therapy and Research. 6 (2): 123–50. doi:10.1007/BF01183887. S2CID   10469356.
  100. 1 2 3 4 Tagay S, Schlottbohm E, Reyes-Rodriguez ML, Repic N, Senf W (January 2014). "Eating disorders, trauma, PTSD, and psychosocial resources". Eating Disorders. 22 (1): 33–49. doi:10.1080/10640266.2014.857517. PMC   3966425 . PMID   24365526.
  101. 1 2 3 4 Reyes-Rodríguez ML, Von Holle A, Ulman TF, Thornton LM, Klump KL, Brandt H, et al. (July 2011). "Posttraumatic stress disorder in anorexia nervosa". Psychosomatic Medicine. 73 (6): 491–497. doi:10.1097/PSY.0b013e31822232bb. PMC   3132652 . PMID   21715295.
  102. 1 2 3 4 5 6 7 8 9 10 Malecki J, Rhodes P, Ussher J (August 2018). "Childhood trauma and anorexia nervosa: from body image to embodiment". Health Care for Women International. 39 (8): 936–951. doi:10.1080/07399332.2018.1492268. PMID   30152723. S2CID   205580678.
  103. "Eating disorders and culture". The Harvard Mental Health Letter. 20 (9): 7. March 2004. PMID   15044128.
  104. Francisco R (2018), "Studies on Body Image, Eating, and Weight in Models, Dancers, and Aesthetic Athletes", in Cuzzolaro M, Fassino S (eds.), Body Image, Eating, and Weight, Springer International Publishing, pp. 401–411, doi:10.1007/978-3-319-90817-5_29, hdl: 10400.14/33058 , ISBN   978-3-319-90817-5, S2CID   150323306
  105. Becker AE (2018). "Sociocultural influences on body image and eating disturbance". In Brownell KD, Walsh BT (eds.). Eating Disorders and Obesity: A Comprehensive Handbook (Third ed.). Guilford Publications. pp. 127–133. ISBN   978-1-4625-3609-2.
  106. Anderson-Fye EP, Becker AE (2004). "Sociocultural Aspects of Eating Disorders". In Thompson KJ (ed.). Handbook of Eating Disorders and Obesity. Hoboken, NJ: John Wiley & Sons. pp. 565–89. ISBN   978-0-471-23073-1.
  107. Baum A (2006). "Eating disorders in the male athlete" (PDF). Sports Medicine. 36 (1): 1–6. doi:10.2165/00007256-200636010-00001. PMID   16445307. S2CID   15296296. Archived (PDF) from the original on 4 June 2015.
  108. Kyriacou O, Treasure J, Schmidt U (January 2008). "Expressed emotion in eating disorders assessed via self-report: an examination of factors associated with expressed emotion in carers of people with anorexia nervosa in comparison to control families". The International Journal of Eating Disorders. 41 (1): 37–46. doi: 10.1002/eat.20469 . PMID   17922532.
  109. Yager J (April 2020). "Managing Patients With Severe and Enduring Anorexia Nervosa: When Is Enough, Enough?". The Journal of Nervous and Mental Disease. 208 (4): 277–282. doi:10.1097/NMD.0000000000001124. PMID   32221180. S2CID   209342890.
  110. "Eating Disorders Anorexia Causes | Eating Disorders". Psychiatric Disorders and Mental Health Issues. 13 June 2014. Archived from the original on 7 March 2016. Retrieved 1 March 2016.
  111. Simpson KJ (February 2002). "Anorexia nervosa and culture". Journal of Psychiatric and Mental Health Nursing. 9 (1): 65–71. doi:10.1046/j.1351-0126.2001.00443.x. PMID   11896858.
  112. Spettigue W, Henderson KA (February 2004). "Eating disorders and the role of the media". The Canadian Child and Adolescent Psychiatry Review. 13 (1): 16–19. PMC   2533817 . PMID   19030149.
  113. Labre MP (April 2002). "Adolescent boys and the muscular male body ideal". The Journal of Adolescent Health. 30 (4): 233–242. doi:10.1016/S1054-139X(01)00413-X. PMID   11927235.
  114. Izydorczyk B, Sitnik-Warchulska K (29 March 2018). "Sociocultural Appearance Standards and Risk Factors for Eating Disorders in Adolescents and Women of Various Ages". Frontiers in Psychology. 9: 429. doi: 10.3389/fpsyg.2018.00429 . PMC   5885084 . PMID   29651268.
  115. Drenten J, Gurrieri L (2018). Crossing the #BIKINIBRIDGE: Exploring the Role of Social Media in Propagating Body Image Trends (1st ed.). 711 Third Avenue, New York, NY 10017: Routledge. ISBN   9781138052550 . Retrieved 15 March 2024.{{cite book}}: CS1 maint: location (link)
  116. 1 2 Norris ML, Boydell KM, Pinhas L, Katzman DK (September 2006). "Ana and the Internet: a review of pro-anorexia websites". The International Journal of Eating Disorders. 39 (6): 443–447. doi:10.1002/eat.20305. PMID   16721839. S2CID   29355957.
  117. 1 2 Lee S (January 1996). "Reconsidering the status of anorexia nervosa as a western culture-bound syndrome". Social Science & Medicine. 42 (1): 21–34. doi:10.1016/0277-9536(95)00074-7. PMID   8745105.
  118. Demarque M, Guzman G, Morrison E, Ahovi J, Moro MR, Blanchet-Collet C (April 2015). "Anorexia nervosa in a girl of Chinese origin: Psychological, somatic and transcultural factors". Clinical Child Psychology and Psychiatry. 20 (2): 276–288. doi:10.1177/1359104513514067. ISSN   1359-1045. PMID   24363225. S2CID   13036347.
  119. Tareen A, Hodes M, Rangel L (February 2005). "Non-fat-phobic anorexia nervosa in British South Asian adolescents". International Journal of Eating Disorders. 37 (2): 161–165. doi:10.1002/eat.20080. ISSN   0276-3478. PMID   15732077.
  120. Kim YR, Nakai Y, Thomas JJ (January 2021). "Introduction to a special issue on eating disorders in Asia". International Journal of Eating Disorders. 54 (1): 3–6. doi:10.1002/eat.23444. ISSN   0276-3478. PMID   33340374. S2CID   229325699.
  121. Kaye WH, Frank GK, Bailer UF, Henry SE, Meltzer CC, Price JC, et al. (May 2005). "Serotonin alterations in anorexia and bulimia nervosa: new insights from imaging studies". Physiology & Behavior. 85 (1): 73–81. doi:10.1016/j.physbeh.2005.04.013. PMID   15869768. S2CID   25676759.
  122. Kaye WH, Bailer UF, Frank GK, Wagner A, Henry SE (September 2005). "Brain imaging of serotonin after recovery from anorexia and bulimia nervosa". Physiology & Behavior. 86 (1–2): 15–17. doi:10.1016/j.physbeh.2005.06.019. PMID   16102788. S2CID   17250708.
  123. Gaudio S, Wiemerslage L, Brooks SJ, Schiöth HB (December 2016). "A systematic review of resting-state functional-MRI studies in anorexia nervosa: Evidence for functional connectivity impairment in cognitive control and visuospatial and body-signal integration". Neuroscience and Biobehavioral Reviews. 71: 578–589. doi: 10.1016/j.neubiorev.2016.09.032 . PMID   27725172.
  124. Fuglset TS, Landrø NI, Reas DL, Rø Ø (2016). "Functional brain alterations in anorexia nervosa: a scoping review". Journal of Eating Disorders. 4: 32. doi: 10.1186/s40337-016-0118-y . PMC   5125031 . PMID   27933159.
  125. Kaye WH, Wagner A, Fudge JL, Paulus M (2011). "Neurocircuitry of Eating Disorders". In Adan RA, Kaye WH (eds.). Behavioral Neurobiology of Eating Disorders: 6. Current Topics in Behavioral Neurosciences. Springer Berlin Heidelberg. pp. 59–80. ISBN   978-3-642-15131-6.
  126. Titova OE, Hjorth OC, Schiöth HB, Brooks SJ (April 2013). "Anorexia nervosa is linked to reduced brain structure in reward and somatosensory regions: a meta-analysis of VBM studies". BMC Psychiatry. 13: 110. doi: 10.1186/1471-244X-13-110 . PMC   3664070 . PMID   23570420.
  127. King JA, Frank GK, Thompson PM, Ehrlich S (February 2018). "Structural Neuroimaging of Anorexia Nervosa: Future Directions in the Quest for Mechanisms Underlying Dynamic Alterations". Biological Psychiatry. 83 (3): 224–234. doi:10.1016/j.biopsych.2017.08.011. PMC   6053269 . PMID   28967386.
  128. Frank GK (August 2015). "Advances from neuroimaging studies in eating disorders". CNS Spectrums. 20 (4): 391–400. doi:10.1017/S1092852915000012. PMC   4989857 . PMID   25902917.
  129. 1 2 3 Mitchell JE, Peterson CB (April 2020). "Anorexia Nervosa". The New England Journal of Medicine. 382 (14): 1343–1351. doi:10.1056/NEJMcp1803175. PMID   32242359. S2CID   214769639.
  130. "DSM-5 Changes: Implications for Child Serious Emotional Disturbance" (PDF). Substance Abuse and Mental Health Services Administration . June 2016. p. 48 (Table 19, DSM-IV to DSM-5 Anorexia Nervosa Comparison). Retrieved 17 September 2021.
  131. Estour B, Galusca B, Germain N (2014). "Constitutional thinness and anorexia nervosa: a possible misdiagnosis?". Frontiers in Endocrinology. 5: 175. doi: 10.3389/fendo.2014.00175 . PMC   4202249 . PMID   25368605.
  132. 1 2 Peat C, Mitchell JE, Hoek HW, Wonderlich SA (November 2009). "Validity and utility of subtyping anorexia nervosa". The International Journal of Eating Disorders. 42 (7): 590–594. doi:10.1002/eat.20717. PMC   2844095 . PMID   19598270.
  133. Singleton JK (12 November 2014). Primary Care, Second Edition: An Interprofessional Perspective. Springer Publishing Company. ISBN   978-0-8261-7147-4 . Retrieved 9 April 2015.
  134. "CBC blood test". MedlinePlus. U.S. National Library of Medicine. Archived from the original on 25 May 2013. Retrieved 31 May 2013.
  135. "Urinalysis". MedlinePlus. U.S. National Library of Medicine. 26 January 2012. Archived from the original on 4 April 2010. Retrieved 4 February 2012.
  136. "Comprehensive metabolic panel". MedlinePlus. U.S. National Library of Medicine. Archived from the original on 5 April 2015. Retrieved 4 February 2012.
  137. Lee H, Oh JY, Sung YA, Chung H, Cho WY (October 2009). "The prevalence and risk factors for glucose intolerance in young Korean women with polycystic ovary syndrome". Endocrine. 36 (2): 326–332. doi:10.1007/s12020-009-9226-7. PMID   19688613. S2CID   207361456.
  138. "Guide to Common Laboratory Tests for Eating Disorder Patients" (PDF). Maudsleyparents.org. Retrieved 29 June 2022.
  139. Montagnese C, Scalfi L, Signorini A, De Filippo E, Pasanisi F, Contaldo F (December 2007). "Cholinesterase and other serum liver enzymes in underweight outpatients with eating disorders". The International Journal of Eating Disorders. 40 (8): 746–750. doi:10.1002/eat.20432. PMID   17610252.
  140. Narayanan V, Gaudiani JL, Harris RH, Mehler PS (May 2010). "Liver function test abnormalities in anorexia nervosa—cause or effect". The International Journal of Eating Disorders. 43 (4): 378–381. doi:10.1002/eat.20690. PMID   19424979.
  141. Walder A, Baumann P (December 2008). "Increased creatinine kinase and rhabdomyolysis in anorexia nervosa". The International Journal of Eating Disorders. 41 (8): 766–767. doi:10.1002/eat.20548. PMID   18521917.
  142. "BUN – blood test". MedlinePlus. U.S. National Library of Medicine. 26 January 2012. Archived from the original on 9 April 2010. Retrieved 4 February 2012.
  143. Sheridan AM, Bonventre JV (July 2000). "Cell biology and molecular mechanisms of injury in ischemic acute renal failure". Current Opinion in Nephrology and Hypertension. 9 (4): 427–434. doi:10.1097/00041552-200007000-00015. PMID   10926180.
  144. Nelsen DA (December 2002). "Gluten-sensitive enteropathy (celiac disease): more common than you think". American Family Physician. 66 (12): 2259–2266. PMID   12507163.
  145. Pepin J, Shields C (February 2012). "Advances in diagnosis and management of hypokalemic and hyperkalemic emergencies". Emergency Medicine Practice. 14 (2): 1–17, quiz 17–8. PMID   22413702.
  146. "Electroencephalogram". Medline Plus. 26 January 2012. Archived from the original on 27 January 2012. Retrieved 4 February 2012.
  147. Misra M, Klibanski A (2011). "The neuroendocrine basis of anorexia nervosa and its impact on bone metabolism". Neuroendocrinology. 93 (2): 65–73. doi:10.1159/000323771. PMC   3214929 . PMID   21228564.
  148. 1 2 3 Nolen-Hoeksema S (2014). "Eating disorders". Abnormal Psychology (Sixth ed.). New York: McGraw-Hill Education. p. 341. ISBN   978-0-07-803538-8.
  149. Striegel-Moore RH, Rosselli F, Perrin N, DeBar L, Wilson GT, May A, et al. (July 2009). "Gender difference in the prevalence of eating disorder symptoms". The International Journal of Eating Disorders. 42 (5): 471–474. doi:10.1002/eat.20625. PMC   2696560 . PMID   19107833.
  150. "Male Anorexia: Understanding Eating Disorders in Men and Boys". Psych Central. 20 May 2022. Retrieved 29 February 2024.
  151. 1 2 Hay PJ, Claudino AM, Touyz S, Abd Elbaky G (27 July 2015). Cochrane Common Mental Disorders Group (ed.). "Individual psychological therapy in the outpatient treatment of adults with anorexia nervosa". Cochrane Database of Systematic Reviews. 2018 (2): CD003909. doi:10.1002/14651858.CD003909.pub2. PMC   6491116 . PMID   26212713.
  152. 1 2 Atti AR, Mastellari T, Valente S, Speciani M, Panariello F, De Ronchi D (May 2021). "Compulsory treatments in eating disorders: a systematic review and meta-analysis". Eating and Weight Disorders. 26 (4): 1037–1048. doi:10.1007/s40519-020-01031-1. PMC   8062396 . PMID   33099675.
  153. 1 2 Lock JD, Fitzpatrick KK (March 2009). "Anorexia nervosa". BMJ Clinical Evidence. 2009. PMC   2907776 . PMID   19445758.
  154. 1 2 National Institute of Mental Health. "Eating disorders". Archived from the original on 23 March 2015. Retrieved 23 March 2015.
  155. Russell GF, Szmukler GI, Dare C, Eisler I (December 1987). "An evaluation of family therapy in anorexia nervosa and bulimia nervosa". Archives of General Psychiatry. 44 (12): 1047–1056. doi:10.1001/archpsyc.1987.01800240021004. PMID   3318754.
  156. Blessitt E, Voulgari S, Eisler I (November 2015). "Family therapy for adolescent anorexia nervosa". Current Opinion in Psychiatry. 28 (6): 455–460. doi:10.1097/yco.0000000000000193. PMID   26382158. S2CID   33438815.
  157. Fisher CA, Skocic S, Rutherford KA, Hetrick SE (1 May 2019). "Family therapy approaches for anorexia nervosa". The Cochrane Database of Systematic Reviews. 2019 (5): CD004780. doi:10.1002/14651858.CD004780.pub4. ISSN   1469-493X. PMC   6497182 . PMID   31041816.
  158. 1 2 le Grange D, Eisler I (January 2009). "Family interventions in adolescent anorexia nervosa". Child and Adolescent Psychiatric Clinics of North America. 18 (1): 159–173. doi:10.1016/j.chc.2008.07.004. PMID   19014864.
  159. 1 2 Treasure J, Parker S, Oyeleye O, Harrison A (May 2021). "The value of including families in the treatment of anorexia nervosa". European Eating Disorders Review. 29 (3): 393–401. doi:10.1002/erv.2816. PMC   8246805 . PMID   33351987.
  160. "Eating Disorders". National Institute of Mental Health (NIMH). 2011. Archived from the original on 1 October 2013. Retrieved 29 September 2013.
  161. Whitfield G, Davidson A (2007). Cognitive Behavioural Therapy Explained. Radcliffe Publishing. ISBN   978-1-85775-603-6 . Retrieved 9 April 2015.
  162. Keltner NL, Steele D (6 August 2014). Psychiatric Nursing. Elsevier Health Sciences. ISBN   978-0-323-29352-5 . Retrieved 9 April 2015.
  163. Tchanturia K, Lounes N, Holttum S (November 2014). "Cognitive remediation in anorexia nervosa and related conditions: a systematic review". European Eating Disorders Review. 22 (6): 454–462. doi:10.1002/erv.2326. PMID   25277720.
  164. Edwards DJ (2017). "An Interpretative Phenomenological Analysis of Schema Modes in a Single Case of Anorexia Nervosa: Part 1- Background, Method, and Child and Parent Modes". Indo-Pacific Journal of Phenomenology. 17: 1–13. doi: 10.1080/20797222.2017.1326728 . S2CID   148977898.
  165. Nolen-Hoeksema S (2014). Abnormal Psychology (Sixth ed.). McGraw-Hill Education. p. 357. ISBN   978-1-259-06072-4.
  166. Garner DM, Garfinkel PE (1 January 1997). Handbook of Treatment for Eating Disorders. Guilford Press. ISBN   978-1-57230-186-3.
  167. Whitnet E, Rolfes SR (2011). Understanding Nutrition. United States: Wadsworth Cengage Learning. p. 255. ISBN   978-1-133-58752-1. Archived from the original on 24 November 2015.
  168. 1 2 3 Garber AK, Sawyer SM, Golden NH, Guarda AS, Katzman DK, Kohn MR, et al. (March 2016). "A systematic review of approaches to refeeding in patients with anorexia nervosa". The International Journal of Eating Disorders. 49 (3): 293–310. doi:10.1002/eat.22482. PMC   6193754 . PMID   26661289.
  169. Kaye WH, Gwirtsman HE, Obarzanek E, George T, Jimerson DC, Ebert MH (October 1986). "Caloric intake necessary for weight maintenance in anorexia nervosa: nonbulimics require greater caloric intake than bulimics". The American Journal of Clinical Nutrition. 44 (4): 435–443. doi:10.1093/ajcn/44.4.435. PMID   3766430.
  170. Dulloo AG, Jacquet J, Girardier L (March 1997). "Poststarvation hyperphagia and body fat overshooting in humans: a role for feedback signals from lean and fat tissues". The American Journal of Clinical Nutrition. 65 (3): 717–723. doi: 10.1093/ajcn/65.3.717 . ISSN   0002-9165. PMID   9062520.
  171. Garfinkel PE, Garner DM (1997). Handbook of Treatment for Eating Disorders. Guilford Press. pp. 156–157. During the weekends in particular, some of the men found it difficult to stop eating. Their daily intake commonly ranged between 8,000 and 10,000 calories. [...] After about 5 months of refeeding, the majority of the men reported some normalization of their eating patterns, but for some the extreme overconsumption persisted. [...] More than 8 months after renourishment began, most men had returned to normal eating patterns; however, a few were still eating abnormal amounts.
  172. Maniscalco J (2007). "Malnutrition: Refeeding Syndrome". In Zaoutis LB, Chiang VW (eds.). Comprehensive Pediatric Hospital Medicine. Elsevier Inc. pp. 633–640 (637–638). doi:10.1016/B978-032303004-5.50103-4. ISBN   978-0-323-03004-5. Archived from the original on 21 January 2024. Hypophosphatemia is considered the hallmark of refeeding syndrome, although other imbalances may occur as well, including hypokalemia and hypomagnesemia.
  173. O'Connor G, Nicholls D (June 2013). "Refeeding hypophosphatemia in adolescents with anorexia nervosa: a systematic review". Nutrition in Clinical Practice. 28 (3): 358–364. doi:10.1177/0884533613476892. PMC   4108292 . PMID   23459608.
  174. "Nutrition support for adults: oral nutrition support, enteral tube feeding and parenteral nutrition". NICE. 4 August 2017. Retrieved 8 March 2021.
  175. 1 2 Pinna F, Sanna L, Carpiniello B (2015). "Alexithymia in eating disorders: therapeutic implications". Psychology Research and Behavior Management. 8: 1–15. doi: 10.2147/PRBM.S52656 . PMC   4278740 . PMID   25565909.
  176. Claudino AM, Hay P, Lima MS, Bacaltchuk J, Schmidt U, Treasure J (January 2006). "Antidepressants for anorexia nervosa". The Cochrane Database of Systematic Reviews (1): CD004365. doi:10.1002/14651858.CD004365.pub2. PMID   16437485.
  177. Meftah AM, Deckler E, Citrome L, Kantrowitz JT (January 2020). "New discoveries for an old drug: a review of recent olanzapine research". Postgraduate Medicine. 132 (1): 80–90. doi:10.1080/00325481.2019.1701823. PMID   31813311. S2CID   208957067.
  178. Arcelus J, Mitchell AJ, Wales J, Nielsen S (July 2011). "Mortality rates in patients with anorexia nervosa and other eating disorders. A meta-analysis of 36 studies". Archives of General Psychiatry. 68 (7): 724–731. doi: 10.1001/archgenpsychiatry.2011.74 . PMID   21727255.
  179. Robinson P (2012). "Avoiding deaths in hospital from anorexia nervosa: the MARSIPAN project". The Psychiatrist. 36 (3): 109–13. doi: 10.1192/pb.bp.111.036699 .
  180. MARSIPAN Working Group (2014). "CR189: Management of Really Sick Patients with Anorexia Nervosa" (Second ed.). Royal College of Psychiatrists. p. 6. Archived from the original on 21 April 2016.
  181. 1 2 3 Conti JE, Joyce C, Hay P, Meade T (October 2020). ""Finding my own identity": a qualitative metasynthesis of adult anorexia nervosa treatment experiences". BMC Psychology. 8 (1): 110. doi: 10.1186/s40359-020-00476-4 . PMC   7583290 . PMID   33092638.
  182. doi: 10.1192/bjo.2018.78
  183. 1 2 3 4 5 6 Graham MR, Tierney S, Chisholm A, Fox JR (March 2020). "The lived experience of working with people with eating disorders: A meta-ethnography" (PDF). The International Journal of Eating Disorders. 53 (3): 422–441. doi:10.1002/eat.23215. PMID   31904870. S2CID   209894802.
  184. Bouquegneau A, Dubois BE, Krzesinski JM, Delanaye P (August 2012). "Anorexia nervosa and the kidney". American Journal of Kidney Diseases. 60 (2): 299–307. doi:10.1053/j.ajkd.2012.03.019. PMID   22609034.
  185. Nolen-Hoeksema S (2014). "Eating Disorders". Abnormal Psychology (Sixth ed.). New York: McGraw Hill Education. p. 342. ISBN   978-0-07-803538-8.
  186. Leigh S (19 November 2019). "Many Patients with Anorexia Nervosa Get Better, But Complete Recovery Elusive to Most". University of California San Francisco. The Regents of The University of California. Retrieved 23 June 2021.
  187. Donaldson AA, Gordon CM (September 2015). "Skeletal complications of eating disorders". Metabolism. 64 (9). Metabolism: Clinical and Experimental: 943–951. doi:10.1016/j.metabol.2015.06.007. PMC   4546560 . PMID   26166318.
  188. Downey AE, Richards A, Tanner AB (3 March 2023). "Linear growth in young people with restrictive eating disorders: "Inching" toward consensus". Frontiers in Psychiatry. 14: 1094222. doi: 10.3389/fpsyt.2023.1094222 . PMC   10020618 . PMID   36937727.
  189. "Core interventions in the treatment and management of anorexia nervosa, bulimia nervosa and related eating disorders" (PDF). National Collaborating Centre for Mental Health. 2004. Archived (PDF) from the original on 27 March 2014.
  190. Vyver E, Steinegger C, Katzman DK (2008). "Eating disorders and menstrual dysfunction in adolescents". Annals of the New York Academy of Sciences. 1135 (1): 253–264. Bibcode:2008NYASA1135..253V. doi:10.1196/annals.1429.013. PMID   18574232. S2CID   42042720.
  191. Devlin MJ, Walsh BT, Katz JL, Roose SP, Linkie DM, Wright L, et al. (April 1989). "Hypothalamic-pituitary-gonadal function in anorexia nervosa and bulimia". Psychiatry Research. 28 (1): 11–24. doi:10.1016/0165-1781(89)90193-5. PMID   2500676. S2CID   39940665.
  192. 1 2 Støving RK, Chen JW, Glintborg D, Brixen K, Flyvbjerg A, Hørder K, et al. (June 2007). "Bioactive insulin-like growth factor (IGF) I and IGF-binding protein-1 in anorexia nervosa". The Journal of Clinical Endocrinology and Metabolism. 92 (6): 2323–2329. doi: 10.1210/jc.2006-1926 . PMID   17389700.
  193. Misra M, Klibanski A (June 2014). "Anorexia nervosa and bone". The Journal of Endocrinology. 221 (3): R163–R176. doi:10.1530/JOE-14-0039. PMC   4047520 . PMID   24898127.
  194. Kleinman R (1 April 2008). Walker's Pediatric Gastrointestinal Disease. PMPH-USA. ISBN   978-1-55009-364-3 . Retrieved 9 April 2015.
  195. 1 2 Norris ML, Harrison ME, Isserlin L, Robinson A, Feder S, Sampson M (March 2016). "Gastrointestinal complications associated with anorexia nervosa: A systematic review". The International Journal of Eating Disorders. 49 (3): 216–237. doi:10.1002/eat.22462. PMID   26407541.
  196. 1 2 3 4 5 6 7 Sachs KV, Harnke B, Mehler PS, Krantz MJ (March 2016). "Cardiovascular complications of anorexia nervosa: A systematic review". The International Journal of Eating Disorders. 49 (3): 238–248. doi:10.1002/eat.22481. PMID   26710932.
  197. 1 2 Goldberg SJ, Comerci GD, Feldman L (January 1988). "Cardiac output and regional myocardial contraction in anorexia nervosa". Journal of Adolescent Health Care. 9 (1): 15–21. doi:10.1016/0197-0070(88)90013-7. PMID   3335466.
  198. Johnson GL, Humphries LL, Shirley PB, Mazzoleni A, Noonan JA (August 1986). "Mitral valve prolapse in patients with anorexia nervosa and bulimia". Archives of Internal Medicine. 146 (8): 1525–1529. doi:10.1001/archinte.1986.00360200083014. PMID   3460535.
  199. 1 2 Frostad S, Rozakou-Soumalia N, Dârvariu Ş, Foruzesh B, Azkia H, Larsen MP, et al. (May 2022). "BMI at Discharge from Treatment Predicts Relapse in Anorexia Nervosa: A Systematic Scoping Review". Journal of Personalized Medicine. 12 (5): 836. doi: 10.3390/jpm12050836 . PMC   9144864 . PMID   35629258.
  200. 1 2 Hasan TF, Hasan H (2011). "Anorexia nervosa: a unified neurological perspective". International Journal of Medical Sciences. 8 (8): 679–703. doi:10.7150/ijms.8.679. PMC   3204438 . PMID   22135615.
  201. Striegel-Moore RH, Rosselli F, Perrin N, DeBar L, Wilson GT, May A, et al. (July 2009). "Gender difference in the prevalence of eating disorder symptoms". The International Journal of Eating Disorders. 42 (5): 471–474. doi:10.1002/eat.20625. PMC   2696560 . PMID   19107833.
  202. Jahrami H, Sater M, Abdulla A, Faris MA, AlAnsari A (June 2019). "Eating disorders risk among medical students: a global systematic review and meta-analysis". Eating and Weight Disorders. 24 (3): 397–410. doi:10.1007/s40519-018-0516-z. PMID   29785631. S2CID   29156560.
  203. Zanetti T (2013). "Epidemiology of Eating Disorders". Eating Disorders and the Skin. pp. 9–15. doi:10.1007/978-3-642-29136-4_2. ISBN   978-3-642-29135-7.
  204. Garber AK, Cheng J, Accurso EC, Adams SH, Buckelew SM, Kapphahn CJ, et al. (December 2019). "Weight Loss and Illness Severity in Adolescents With Atypical Anorexia Nervosa". Pediatrics. 144 (6). doi:10.1542/peds.2019-2339. PMC   6889949 . PMID   31694978.
  205. Makino M, Tsuboi K, Dennerstein L (September 2004). "Prevalence of eating disorders: a comparison of Western and non-Western countries". MedGenMed. 6 (3): 49. PMC   1435625 . PMID   15520673.
  206. Tsai G (December 2000). "Eating disorders in the Far East". Eating and Weight Disorders. 5 (4): 183–197. doi:10.1007/BF03354445. PMID   11216126. S2CID   41396054.
  207. 1 2 Bonci CM, Bonci LJ, Granger LR, Johnson CL, Malina RM, Milne LW, et al. (2008). "National athletic trainers' association position statement: preventing, detecting, and managing disordered eating in athletes". Journal of Athletic Training. 43 (1): 80–108. doi:10.4085/1062-6050-43.1.80. PMC   2231403 . PMID   18335017.
  208. Thiel A, Gottfried H, Hesse FW (October 1993). "Subclinical eating disorders in male athletes. A study of the low weight category in rowers and wrestlers". Acta Psychiatrica Scandinavica. 88 (4): 259–265. doi:10.1111/j.1600-0447.1993.tb03454.x. PMID   8256643. S2CID   10232724.
  209. Crilly L (2 April 2012). Hope with Eating Disorders. Hay House, Inc. ISBN   978-1-84850-906-1 . Retrieved 9 April 2015.
  210. Thomas JJ, Vartanian LR, Brownell KD (May 2009). "The relationship between eating disorder not otherwise specified (EDNOS) and officially recognized eating disorders: meta-analysis and implications for DSM". Psychological Bulletin. 135 (3): 407–433. doi:10.1037/a0015326. PMC   2847852 . PMID   19379023.
  211. 1 2 3 4 5 6 7 8 9 Landi F, Calvani R, Tosato M, Martone AM, Ortolani E, Savera G, et al. (January 2016). "Anorexia of Aging: Risk Factors, Consequences, and Potential Treatments". Nutrients. 8 (2): 69. doi: 10.3390/nu8020069 . PMC   4772033 . PMID   26828516.
  212. 1 2 3 4 Ekern B (25 February 2016). "Common Types of Eating Disorders Observed in the Elderly Population". Eating Disorder Hope. Retrieved 12 June 2022.
  213. 1 2 3 4 Donini LM, Poggiogalle E, Piredda M, Pinto A, Barbagallo M, Cucinotta D, et al. (2 May 2013). "Anorexia and eating patterns in the elderly". PLOS ONE. 8 (5): e63539. Bibcode:2013PLoSO...863539D. doi: 10.1371/journal.pone.0063539 . PMC   3642105 . PMID   23658838.
  214. 1 2 Lapid MI, Prom MC, Burton MC, McAlpine DE, Sutor B, Rummans TA (June 2010). "Eating disorders in the elderly". International Psychogeriatrics. 22 (4): 523–536. doi:10.1017/S1041610210000104. PMID   20170590. S2CID   38114971.
  215. 1 2 3 4 Morley JE, Silver AJ (1 January 1988). "Anorexia in the elderly". Neurobiology of Aging. 9 (1): 9–16. doi:10.1016/S0197-4580(88)80004-6. PMID   2898107. S2CID   3099767.
  216. Lau S, Pek K, Chew J, Lim JP, Ismail NH, Ding YY, et al. (September 2020). "The Simplified Nutritional Appetite Questionnaire (SNAQ) as a Screening Tool for Risk of Malnutrition: Optimal Cutoff, Factor Structure, and Validation in Healthy Community-Dwelling Older Adults". Nutrients. 12 (9): 2885. doi: 10.3390/nu12092885 . PMC   7551805 . PMID   32967354.
  217. "Functional Assessment of Anorexia/Cachexia Treatment (FAACT)". FACIT.org.
  218. Devriendt E, Wellens NI, Flamaing J, Declercq A, Moons P, Boonen S, et al. (September 2013). "The interRAI Acute Care instrument incorporated in an eHealth system for standardized and web-based geriatric assessment: strengths, weaknesses, opportunities and threats in the acute hospital setting". BMC Geriatrics. 13: 90. doi: 10.1186/1471-2318-13-90 . PMC   3766642 . PMID   24007312.
  219. 1 2 Pearce JM (2004). "Richard Morton: origins of anorexia nervosa". European Neurology. 52 (4): 191–192. doi:10.1159/000082033. PMID   15539770. S2CID   30482453.
  220. Espi Forcen F (April 2013). "Anorexia mirabilis: the practice of fasting by Saint Catherine of Siena in the late Middle Ages". The American Journal of Psychiatry. 170 (4): 370–371. doi:10.1176/appi.ajp.2012.12111457. PMID   23545792.
  221. Harris JC (November 2014). "Anorexia nervosa and anorexia mirabilis: Miss K. R--and St Catherine Of Siena". JAMA Psychiatry. 71 (11): 1212–1213. doi:10.1001/jamapsychiatry.2013.2765. PMID   25372187.
  222. 1 2 Gull WW (1894). Acland TD (ed.). Medical Papers. p. 309.
  223. King NA, Burley VJ, Blundell JE (October 1994). "Exercise-induced suppression of appetite: effects on food intake and implications for energy balance". European Journal of Clinical Nutrition. 48 (10). United States government: 715–724. PMID   7835326. Subjective feelings of hunger were significantly suppressed during and after intense exercise sessions (P 0.01), but the suppression was short-lived.
  224. Grant JE, Phillips KA (2004). "Is anorexia nervosa a subtype of body dysmorphic disorder? Probably not, but read on". Harvard Review of Psychiatry. 12 (2): 123–126. doi:10.1080/10673220490447236. PMC   1622894 . PMID   15204807.
  225. Gull WW (September 1997). "Anorexia nervosa (apepsia hysterica, anorexia hysterica). 1868". Obesity Research. 5 (5): 498–502. doi: 10.1002/j.1550-8528.1997.tb00677.x . PMID   9385628.
  226. Lasègue E (6 September 1873). "On Hysterical Anorexia". Medical Times and Gazette. See also "On hysterical anorexia (a). 1873". Obesity Research. 5 (5): 492–497. September 1997. doi: 10.1002/j.1550-8528.1997.tb00676.x . PMID   9385627.
  227. Arnold C (2012). Decoding Anorexia: How Breakthroughs in Science Offer Hope for Eating Disorders. Routledge Press. ISBN   978-0-415-89867-6.
  228. Arnold C (29 March 2016). "Anorexia: you don't just grow out of it". The Guardian. Archived from the original on 29 March 2016. Retrieved 29 March 2016.

Further reading

Why do anorexia patients feel fat? — Anouk Keizer (Utrecht University)